Which Parent Determines a Child’s Blood Type?

Both parents contribute equally to a child’s blood type. There is no single parent whose genes override the other’s. A child inherits one copy of the ABO blood group gene from each parent, and the combination of those two copies, along with how the gene variants interact, produces the child’s final blood type. The same holds for the Rh factor (positive or negative) and dozens of other blood group systems. The real complexity lies not in which parent matters more, but in how particular gene combinations can produce results that seem to defy the family tree.

How ABO Blood Type Is Inherited

Your ABO blood type is determined by a single gene on chromosome 9. That gene codes for an enzyme (a glycosyltransferase) that attaches a specific sugar molecule to the surface of red blood cells. The A version of the gene adds one kind of sugar, producing the A antigen, while the B version adds a different sugar, producing the B antigen. The O version produces a nonfunctional enzyme that doesn’t add anything, leaving only a precursor structure called the H antigen on the cell surface.¹

Because you carry two copies of this gene, one from each parent, there are six possible genetic combinations: AA, AO, BB, BO, AB, and OO. The A and B versions are codominant with each other, meaning if you inherit an A from one parent and a B from the other, both sugars get placed on your red blood cells and you are type AB. Both A and B are dominant over O, so a person with AO genes tests as type A, and someone with BO genes tests as type B. Only a person who inherits O from both parents ends up as type O.

This is why two parents who are both type A can have a type O child. If both carry the hidden O copy (genotype AO), there’s a chance their child inherits the O from each of them. It isn’t that one parent’s genes “won.” Both parents handed over the same variant, and that combination produced the result.

Why Certain Parent Combinations Surprise People

The most common source of confusion is the gap between what a blood test reports (the phenotype) and what a person actually carries genetically (the genotype). A parent who tests as type A could be AA or AO. A parent who tests as type B could be BB or BO. You can’t tell from a standard blood test which one it is. That hidden O allele only reveals itself when it meets another O from the other parent.

Here are some combinations that catch people off guard:

• Two type A parents, type O child: Both parents are AO. The child got O from each.
• Type A and type B parents, type O child: One parent is AO, the other is BO. The child inherited O from both.
• Two type O parents: Every child will be type O. There is no A or B allele to pass along.
• Type AB parent: Can never have a type O child, because every child gets either an A or a B from that parent. But both type A and type B children are possible, depending on what the other parent contributes.

These patterns are entirely predictable once you know the parents’ genotypes, but since routine blood typing only reveals the phenotype, the results can seem puzzling.

The Rh Factor Is a Separate Inheritance

The positive or negative label in your blood type (A+, O−, etc.) refers to the Rh D antigen, which is controlled by a completely different gene on chromosome 1. Two closely linked genes, RHD and RHCE, govern the Rh system, and together they account for the most clinically complex blood group system after ABO.² The RHD gene determines whether you are Rh-positive or Rh-negative. Having at least one working copy of RHD makes you positive; being negative means you carry two nonfunctional or deleted copies.

Because Rh-positive is dominant over Rh-negative, two Rh-positive parents can have an Rh-negative child if both carry one silent copy of the nonfunctional gene. Two Rh-negative parents, on the other hand, will always have Rh-negative children. This mirrors the logic of ABO: both parents contribute, neither dominates, and hidden copies can produce surprises.

When Parent and Baby Blood Types Clash

One area where the specific pairing of mother and child matters a great deal is blood type incompatibility during pregnancy. The most well-known form involves the Rh factor. If an Rh-negative mother carries an Rh-positive baby (the baby having inherited the positive gene from the father), the mother’s immune system can develop antibodies against the baby’s red blood cells. This doesn’t usually cause problems in a first pregnancy, but in subsequent pregnancies those antibodies can cross the placenta and attack the baby’s blood cells, leading to hemolytic disease of the newborn.³

Standard prevention involves giving Rh-negative mothers an injection of anti-D immunoglobulin around 28 to 30 weeks of pregnancy, with a second dose within 72 hours after birth if the newborn is Rh-positive.⁴ This treatment has dramatically reduced the incidence of Rh disease over the past several decades.

ABO incompatibility is more common but usually milder. The classic scenario is a type O mother carrying a type A or type B baby. Type O mothers naturally produce anti-A and anti-B antibodies, which can sometimes cross the placenta and cause mild jaundice in the newborn. It rarely requires aggressive treatment.⁵ When it does cause problems, the jaundice tends to show up a day or two after birth and is typically managed with phototherapy. More severe outcomes are possible but uncommon, and infants with a positive direct antiglobulin test are at higher risk of significant jaundice than those who test negative.⁶

Rare Exceptions That Break the Standard Rules

Genetics textbooks present blood type inheritance as a clean, predictable system. In most families it works exactly that way. But a handful of rare genetic situations can produce results that seem impossible under the standard rules.

Cis-AB

In typical AB inheritance, one parent supplies the A allele and the other supplies B. In cis-AB, both the A and B activities come from a single allele inherited from one parent.⁷ That means a parent who carries a cis-AB allele paired with an O allele can test as type AB yet have a child who is type O — something ordinarily considered impossible. If the child inherits the O allele from that parent and another O from the other parent, the child ends up type O despite having an AB parent.⁸ This variant is quite rare globally, though it appears somewhat more frequently in certain East Asian populations. In some cis-AB cases, either the A or the B component may be weakly expressed or even absent on standard testing, adding another layer of confusion.⁹

Chimerism

Chimerism occurs when a person carries two genetically distinct cell populations, often from the fusion of two fraternal twin embryos very early in development. In blood typing, this shows up as “mixed-field” reactions: some red blood cells react with one antibody and others don’t. A person might appear to carry blood group B, but molecular analysis reveals a mixture of B and O cell populations at unequal ratios.¹⁰ In some cases the degree of chimerism is so low — less than 1% of cells — that it can only be detected with highly sensitive molecular testing.¹¹ These cases are genuinely rare, but they can create headaches in blood banks and have historically prompted false suspicions of sample mix-ups or even questioned parentage.

Weak Subgroups

Not all A or B alleles produce the same strength of antigen on the cell surface. Some variants result in much weaker expression, and a person with a weak A subgroup (like A3) might initially test as type O on a routine screen. Molecular analysis of these weak subgroups has revealed that they can arise from different underlying mutations in the same gene, so two people with the same “A3” phenotype might carry different genetic changes.¹² A child who inherits one of these weak alleles may appear to have a blood type that doesn’t match the expected pattern from the parents, though the inheritance itself followed the standard rules.

Blood Type Can Appear to Change

While your blood type is genetically fixed at conception, certain diseases can suppress the expression of blood group antigens on your red blood cells. The best-documented examples come from acute myeloid leukemia, where patients have had their A or B antigens weaken or vanish entirely during the active phase of the disease, only to reappear when the leukemia went into remission.¹³ The underlying DNA hasn’t changed; the leukemic cells simply fail to produce the enzymes that normally put the antigens on the cell surface.¹⁴

Research into why this happens points to epigenetic regulation. The ABO gene’s promoter region can be silenced through a chemical modification called methylation, which switches the gene off without altering the DNA sequence itself. In lab experiments, treating cells with a demethylating agent reactivated the A gene and restored antigen expression.¹⁵ This means your blood type, while genetically determined by both parents, depends on the gene actually being “turned on” in your blood-forming cells. In nearly everyone, it is. In a small number of leukemia patients, it temporarily isn’t.

More Than Just ABO and Rh

When people ask about blood type, they usually mean ABO and Rh. But the International Society of Blood Transfusion recognizes around 30 blood group systems, each controlled by its own gene or gene cluster, and each inherited from both parents in the same way.¹⁶ Systems like Kell, Kidd, Duffy, MNS, and Lewis are clinically significant because mismatches can cause transfusion reactions or contribute to hemolytic disease in newborns. Each follows its own inheritance pattern, but all share the same basic principle: one allele from mom, one from dad, neither parent’s contribution inherently outweighing the other’s.

The Duffy blood group system is a particularly interesting example. It acts as a receptor for the malaria parasite Plasmodium vivax, and in many populations of sub-Saharan African ancestry, a variant that silences Duffy expression on red blood cells has become very common, conferring natural resistance to that species of malaria.¹⁷ Like ABO and Rh, Duffy status is inherited from both parents.

Your Blood Type in Places Other Than Blood

About 80% of people are “secretors,” meaning they also express their ABO blood group antigens in saliva, mucus, and other body fluids. Whether you are a secretor depends on yet another gene, FUT2, which codes for an enzyme that places the H antigen on secretory tissues.¹⁸ If both copies of your FUT2 gene are nonfunctional, you are a non-secretor: your red blood cells still carry the expected ABO antigens, but your saliva doesn’t. The FUT2 gene is separate from the ABO gene, inherited independently from both parents.¹⁹

Secretor status has practical implications. In forensic science, saliva samples from secretors can help identify ABO type. In medicine, secretor status has been linked to differences in gut microbiome composition and susceptibility to certain infections, including norovirus. The key point for inheritance is that secretor status is one more trait where both parents contribute equally, and non-secretor status only appears when a child inherits the nonfunctional variant from both sides.

Blood Type and Paternity Testing

Before DNA testing became widely available, blood typing was one of the few tools available to resolve paternity disputes. The logic was straightforward: if a child’s blood type was impossible given the mother’s and alleged father’s types, the man could be excluded. A type O child with a type AB alleged father, for instance, is strong evidence against paternity under normal circumstances.

However, ABO phenotyping alone is a fairly blunt instrument. It can exclude some men but can never confirm that a particular man is the father, because many people share the same blood type. ABO genotyping — looking at the actual DNA sequence rather than just which antigens appear on the cells — improves the ability to distinguish individuals, but even genotyping of the ABO locus alone is not sufficient for reliable paternity testing.²⁰ Modern paternity tests use panels of many genetic markers across the genome, making ABO typing essentially a historical curiosity in this context. The rare exceptions described earlier, cis-AB and chimerism, also made blood-type-based paternity calls unreliable in edge cases even before DNA testing replaced the approach.

Why Blood Types Exist at All

Given that blood type mismatches can cause disease in newborns and dangerous transfusion reactions, you might wonder why evolution hasn’t settled on a single universal blood type. The persistence of A, B, and O alleles across human populations, and even across primate species, suggests that maintaining this diversity offers some survival advantage.

The ABO polymorphism is ancient. Genetic studies show that the A and B gene variants were present before the evolutionary lineages leading to humans, chimpanzees, gorillas, and orangutans diverged, placing the polymorphism at more than 13 million years old.²¹ Analysis of genetic variation in humans and gibbons supports the idea that the A and B blood groups are a “trans-species polymorphism” maintained by balancing selection over tens of millions of years, making it one of the oldest known examples of such selection in primates outside of the immune system’s major histocompatibility complex.²²

One leading hypothesis for why this diversity persists involves malaria. Research has clarified that non-O blood groups are significant risk factors for life-threatening falciparum malaria, because infected red blood cells form clumps (rosettes) more readily with A, B, or AB cells than with O cells.²³ Type O appears to offer some protection against severe malaria through reduced rosetting.²⁴ If type O were universally advantageous, you’d expect it to have swept through all human populations, but A and B alleles persist at high frequencies, implying they confer their own advantages against other pathogens or in other contexts that researchers are still working to pin down.

The global distribution of blood types reflects these competing selective pressures. Type O is most common worldwide, but the proportions of A and B vary enormously by region. Indigenous populations in Central and South America are overwhelmingly type O, while type B reaches its highest frequencies in Central and South Asia. These patterns are the result of millions of years of both parents, generation after generation, shuffling the same ancient set of alleles into new combinations shaped by local disease pressures, genetic drift, and migration.