It is well accepted in clinical medicine that there is wide variation between patients in the handling of and response to drugs; these differences are based in part on genetic mechanisms. Pharmacogenetic differences among patients contribute to altered drug kinetics, resulting in failure of therapy or in side effects related to blood levels after standard doses. Predisposition to idiosyncratic reactions (hepatotoxicity, aplastic anemia, or even carcinogenesis) may also be genetically determined.1 Similarly, not all fetuses exposed to a potential teratogen in utero will have birth defects, and the pattern of any abnormalities may vary. Some of the differences may result . . .