So traditional Mendelian genetics assume that each trait is determined by one gene, and that that gene has two alleles and those two alleles are obviously dominant and recessive. What happens when we violate these assumptions? Well there are several common outcomes. First, the dominant allele doesn't always completely mask the recessive allele in a heterozygote. You might example see this in a flower's color. If an enzyme is responsible for making some pigment in the flower, then the amount that enzyme is expressed might change the flower color. And so you could imagine that a homozygous dominant where there are two copies of a functional enzyme might result in a red flower, whereas a homozygous recessive where none of that functional enzyme is being created might result in no pigment and give us a white color, but perhaps a heterozygote where there's only one allele that's creating a functional enzyme. Maybe that will give us a pink flower. And so we call this incomplete dominance. The other assumption that is routinely broken is that there are only two alleles per gene. And we know from our discussion of polymorphisms that there are often more than two alleles at a particular locus, and the most famous example of this in humans is the ABO locus, which determines whether your blood type is A or B or O. And there are three alleles here. There's allele IA. There's allele IB. And there's allele little I. And these alleles encode enzymes that determine the polysaccharides, right, the sugar groups on the outside of red blood cells. And the compatibility between the blood types of, say, a blood donor and the recipient of donated blood is really important for safe blood transfusions. And so this IA allele encodes an enzyme that makes a polysaccharide called the Aantigen. And if you have the Aantigen on the outside of your red blood cells, then you have type A. Blood similarly the IB allele encodes a slightly different enzyme that makes a polysaccharide on the outside of your red blood cells called the Bantigen. And the little I allele is a non-functional enzyme, right? And so this produces no antigens. It does not modify those polysaccharides on the outside of the red blood cell. And now that we know something about the molecular biology of this setup, we can see how these alleles interact, right? And the homozygodes are easy, right? If you're homozygous IA, IA, then you're going to have type A blood. If you're homozygous IB, IB, you're going to have type B blood. And if you're homozygous little I, little I, you're going to have type O blood because you won't have any functional enzyme here to make the Aantigen or the Bantigen. It's also clear based on this molecular biology, what some of the heterozygodes look like, right? If you are IA, little I, you have one allele that is making an enzyme that makes that Aantigen. And so you'll have type A blood. If you are a heterozygode IB, little I, you'll have one allele that is making an enzyme that makes this Bantigen. And you'll have type B blood. But it's the IA, IB heterozygode that's really interesting because now you'll have one allele that's making an enzyme that's making the Aantigen and one allele that is making the enzyme that's making the Bantigen and your blood type is type A B. And so this situation where both alleles have a phenotype result that's expressed in the heterozygode, we call this situation co-dominance. Before we round out the chapter with another look at probability and inheritance, we need to consider one more molecular reason that the inheritance of traits might not be strictly Mendelian and that's epistasis.