So I counseled patients that these children may need some surgical correction of those hernias later in life. Well, I think a couple of things are coming down the pike. We had our center of development animal model for this disease, and we feel that we sort of looked for only one a sign of disease, that of the fetal anemia. We really are interested in trying to get rid of the maternal antibody, that's the problem. If we could get a mother to drop her titers before she became pregnant through some sort of immunomodulation, we think that would ultimately be the correct way to treat this disease.
Studies are early.
The model is clearly a representative of human disease, and we are encouraged that we may one day be able to treat these mothers in essence and not have to do intrauterine transfusions. In some situations even today, through genetic engineering, we are now able to offer some unique therapies to the father or to the couple that are in fact heterozygous. Just for a second, let me explain that. If the father is heterozygous, that means that although he is Rh positive, he has a 50-50 chance of in fact fathering an affected offspring, and if that offspring happens to be Rh negative, of course, then that offspring has no effects of the disease and he'll be fine. If in fact the offspring is Rh positive, he obviously will be affected.