What Causes Moles and Skin Tags to Appear?

Moles and skin tags arise from different biological processes, though both are among the most common benign skin growths. Moles form when pigment-producing cells called melanocytes cluster together instead of spreading evenly through the skin, driven by specific gene mutations and amplified by sun exposure. Skin tags grow from a different cell type entirely, fed by friction and metabolic signals like excess insulin. Understanding what triggers each one reveals why some people seem to collect dozens while others have almost none.

The Gene Mutations Behind Moles

Most common moles owe their existence to a mutation in a gene called BRAF. When this gene picks up a specific activating change, it sends a constant “grow” signal to melanocytes, causing them to multiply and cluster into the small pigmented spots we recognize as moles. Researchers confirmed this by introducing the same human BRAF mutation into zebrafish embryos: about ten percent of injected fish developed focal clusters of heavily pigmented melanocytes as adults, ranging from small discrete spots to patches covering large portions of their bodies. Critically, these clusters looked well-differentiated and showed no signs of invasion into surrounding tissue, behaving like a human mole rather than a cancer.¹

BRAF is not the only player. Different types of moles tend to carry different mutations. Acquired moles, the kind that show up during childhood and young adulthood, most often harbor BRAF changes. Spitz nevi are associated with HRAS mutations, blue nevi with GNAQ mutations, and congenital moles with NRAS mutations.² Each mutation activates cell growth through a shared signaling pathway, but the specific gene involved helps determine the mole’s appearance and behavior.

A natural question follows: if these mutations tell melanocytes to keep dividing, why don’t all moles become cancerous? The answer is a built-in safety brake called oncogene-induced senescence. When the growth signal from a mutation like BRAF becomes too strong, cells activate tumor-suppressor pathways that force them into a permanent state of growth arrest. The melanocytes stay alive and pigmented but stop dividing, which is why most moles grow to a certain size and then simply sit there for years.³ Progression to melanoma requires additional mutations that knock out those safety brakes.

Why Sun Exposure Multiplies Mole Count

Genetics load the gun, but ultraviolet light pulls the trigger for many acquired moles. A large study of Australian schoolchildren found that mole counts climbed steadily as you moved toward the equator, from an average of about 51 moles per child in Melbourne to roughly 77 in tropical Townsville. That latitude gradient persisted even after accounting for skin color, hair color, eye color, and freckling tendency, pointing to UV exposure itself as the driving factor.⁴

A separate study of children in the United Kingdom reinforced the picture from a different angle. Among white children, overall skin color had little influence on how many moles they developed. What did matter was a tendency to burn rather than tan, a history of actual sunburns, and a lifestyle involving more outdoor sun. Most striking was a strong positive link between mole count and the number of holidays taken in sunny climates, independent of whether those holidays produced a sunburn.⁵ In other words, cumulative UV dosage during childhood seems to be the key ingredient, not just dramatic sunburn episodes.

This helps explain a pattern many people notice: moles appear mostly on sun-exposed areas like the arms, face, and upper back, and most new moles show up before age 30, during the years when cumulative sun damage is still climbing steeply. It also means that childhood sun protection has an outsized effect on lifetime mole count.

Moles You Are Born With

Congenital moles, visible at birth or appearing within the first few months of life, have a distinct origin. Rather than arising from UV damage accumulated over years, they trace back to a mutation that occurs spontaneously in a single cell during fetal development. Because the mutation happens after the fertilized egg has already begun dividing, it shows up only in the descendant cells of that one mutant cell, not in the rest of the body. This pattern is called mosaicism.

Research on children with multiple large congenital moles found that the responsible mutation sat in codon 61 of the NRAS gene in the majority of cases. The mutation appeared in affected skin and, when neurological tissue was involved, in brain lesions as well, but was absent from the patient’s blood and unaffected skin, confirming that it arose after conception rather than being inherited from a parent.⁶ About 70 percent of multiple congenital mole cases trace to NRAS.⁷

For the remaining cases, researchers have identified mosaic fusions involving the BRAF and RAF1 genes. These fusions lose the regulatory portion of the gene but keep the kinase domain intact, essentially stripping away the cell’s ability to control growth signaling. One study confirmed the fusions in multiple separate moles on the same patient while finding them absent from blood, reinforcing that a single early embryonic event seeded the melanocyte expansion that later became visible as scattered congenital moles.⁸

Do Moles Come and Go With Hormones?

A persistent belief holds that pregnancy darkens and enlarges moles because of surging hormones. There is a kernel of biological logic here: pregnancy increases levels of melanocyte-stimulating hormone, estrogen, and progesterone, all of which can stimulate pigment production. Older medical literature supported the idea that these hormonal shifts caused visible changes in moles. However, more recent and methodologically stronger studies suggest that pregnancy itself does not produce significant changes in most moles.⁹ Some darkening of surrounding skin, particularly along the midline of the abdomen or around the nipples, is well documented during pregnancy, but that is generalized hyperpigmentation rather than a mole-specific change.

That said, any mole that changes noticeably during pregnancy, or at any other time, deserves a dermatologist’s evaluation, because the features that signal a problematic mole (asymmetry, irregular borders, color variation, increasing diameter) are the same regardless of hormonal context.

Why Moles Fade With Age

If you have ever noticed that elderly relatives seem to have fewer dark moles than middle-aged ones, that is not your imagination. Population-level data show that the average number of moles per person decreases over time starting around age 20. Researchers estimating transformation rates calculated that individual moles disappear at a steady rate each year, with the rate slightly higher in women than in men.¹⁰ The melanocytes in an aging mole gradually lose their pigment or are replaced by fibrous tissue, causing the mole to flatten and lighten until it effectively vanishes. This is the natural endpoint of the senescence process described earlier: the growth-arrested melanocytes eventually wind down entirely.

What Causes Skin Tags

Skin tags are a fundamentally different growth. While moles are clusters of pigment cells, skin tags are stalked pouches of normal skin, typically containing collagen fibers, small blood vessels, and a covering of epidermis. They favor warm, moist areas where skin rubs against itself or against clothing: the neck, armpits, groin folds, under the breasts, and along the eyelids. Friction is widely considered the primary mechanical trigger, which is why skin tags become more common with weight gain and during pregnancy when body contours change and skin folds deepen.

But friction alone does not fully explain the pattern. If it did, manual laborers with calloused hands would be covered in skin tags, and they are not. The growth signals that actually drive skin tag formation appear to come from inside the body.

Insulin Resistance and Metabolic Signals

The strongest metabolic predictor of skin tags is insulin resistance. When insulin levels run chronically high, as they do in type 2 diabetes and metabolic syndrome, the excess insulin activates growth factor receptors on fibroblasts and epidermal cells. This stimulates both cell types to proliferate, and since fibroblasts and epidermis are the main structural components of a skin tag, the connection is direct.¹¹

A case-control study from eastern India put numbers to the relationship: patients with skin tags were roughly eleven times more likely to meet criteria for metabolic syndrome compared with controls. Specifically, larger waist circumference and low HDL cholesterol showed the strongest independent associations with skin tags after adjusting for other variables.¹² A separate study found additional links to elevated cholesterol, elevated triglycerides, and hypothyroidism, with high cholesterol showing a significant independent association even in multivariate analysis.¹³

This metabolic connection has a practical implication that many people miss: a sudden crop of skin tags, especially in someone who has not gained significant weight, can be an early visible sign of insulin resistance or prediabetes. Some dermatologists use prominent skin tags, particularly when accompanied by darkened, velvety skin patches in the same fold areas, as a prompt to check blood sugar and lipid levels.

Excess Growth Hormone and Skin Tags

The insulin connection has a parallel in conditions involving excess growth hormone. In acromegaly, a disorder caused by a growth-hormone-secreting pituitary tumor, skin changes are among the most visible features. Chronically elevated growth hormone and its downstream mediator, insulin-like growth factor 1, act directly on skin cells and their supporting structures, promoting overgrowth. Pigmented skin tags and darkened velvety skin patches are frequently observed in acromegaly patients.¹⁴ The shared thread between insulin resistance and acromegaly is growth factor signaling: both conditions flood skin cells with proliferative signals, and skin tags are one result.

Research on actively growing skin tags has found elevated levels of epidermal growth factor receptors compared to skin tags that have stopped growing, supporting the idea that growth factor signaling is the engine behind their formation and expansion.¹⁵

Does HPV Play a Role in Skin Tags?

A widely cited early study detected human papillomavirus DNA, specifically types 6 and 11, in 88 percent of skin tag samples, leading to the hypothesis that HPV infection might contribute to skin tag formation in much the same way it causes warts.¹⁶ If true, this would make skin tags partly infectious in origin.

However, later studies have failed to replicate this finding. One investigation tested skin tag samples for both low-risk and high-risk HPV subtypes and found that all samples in both the skin tag group and the control group were negative for low-risk HPV, with no significant difference between groups or across age and sex categories.¹⁷ The discrepancy likely reflects differences in testing sensitivity and contamination risk between older PCR methods and newer ones. At present, the evidence does not support treating HPV as a major cause of typical skin tags, though the question has not been definitively closed.

Pigmentation Genes and Individual Susceptibility

Beyond the specific mutations that create individual moles, broader genetic variation in pigmentation genes shapes how many moles a person is likely to develop over a lifetime. Researchers studying twins in Queensland, Australia, examined variants in the MC1R gene, which plays a central role in determining hair color, skin color, and freckling tendency. They found statistical associations between specific MC1R variants and mole count, suggesting that the same genetic architecture that gives someone red hair or fair skin also predisposes them to developing more moles.¹⁸ This helps explain why mole count runs in families even apart from specific environmental exposures like sun.

The interplay between pigmentation genes and UV exposure is worth understanding practically. Fair-skinned individuals with certain MC1R variants produce less of the protective eumelanin pigment and more of the less protective pheomelanin. Their melanocytes are more vulnerable to UV-induced DNA damage, which increases the chance of acquiring the BRAF or NRAS mutations that seed new moles. So genetics and environment are not independent risk factors; they amplify each other.

When the Immune System Erases a Mole

Sometimes a mole develops a pale ring around it and gradually fades from the center outward. This is a halo nevus, and it represents the immune system actively destroying the melanocytes that make up the mole. Research points to CD8+ T cells as the likely agents of destruction: they infiltrate the mole, recognize melanocyte proteins as targets, and kill the pigment cells in a process that closely resembles how the immune system attacks melanocytes in vitiligo or in regressing melanoma.¹⁹²⁰

What triggers this immune attack in certain moles but not others remains unclear. The white halo surrounding the fading mole is itself a zone of depigmentation caused by collateral immune damage to normal melanocytes near the mole. Interestingly, recent research has identified a regulatory mechanism involving neutrophils expressing PD-L1, a checkpoint molecule, that appears to help rein in the immune response and prevent the depigmentation from spreading indefinitely.²¹ Halo nevi are most common in teenagers and young adults, are almost always benign, and tend to resolve on their own over months to years.

Mole Subtypes and Where They Sit in the Skin

Moles are not all structurally identical, and the differences matter when a dermatologist evaluates one. The melanocyte clusters that form a mole can sit at different depths within the skin, and the position shifts as a mole ages:

• Junctional nevi: melanocytes clustered right at the junction between the outer epidermis and the deeper dermis. These tend to be flat and darkly pigmented.
• Compound nevi: melanocytes found in both the junction and the dermis below. These are often slightly raised with mixed coloring.
• Dermal nevi: melanocytes that have migrated entirely into the dermis. These are typically dome-shaped, lighter in color, and sometimes flesh-toned.

The progression from junctional to compound to dermal roughly tracks a mole’s life cycle, moving deeper and losing pigment over time. This structural classification also determines which removal approaches work best for cosmetic concerns. Junctional nevi, being superficial, respond to pigment-targeting lasers, while compound and dermal nevi may require ablative techniques that reach deeper tissue.²² This is why a flat brown mole on your arm and a raised flesh-colored bump on your neck can both be “moles” despite looking nothing alike.

Skin Tags in Pregnancy

Skin tags frequently appear during the second and third trimesters of pregnancy, and unlike the debatable effect of pregnancy hormones on moles, this phenomenon has a clearer explanation. Pregnancy induces a state of physiological insulin resistance: the body reduces its sensitivity to insulin to ensure that circulating glucose stays available for the growing fetus. This means insulin levels rise, activating the same growth factor pathways that drive skin tag formation in people with metabolic syndrome. Combined with weight gain that deepens skin folds and increases friction, pregnancy creates ideal conditions for new skin tags. Most pregnancy-related skin tags persist after delivery but do not continue growing once insulin sensitivity normalizes postpartum.