The inhibition of characteristic CYP2C9 and CYP2C19 activities (diclofenac and S-mephenytoin hydroxylation) by AML was studied using genotyped microsomes corresponding to extensive enzyme activity (wild-type alleles), intermediate activity, and no (or poor) activity, as specified in Table 5. This evidence concerns the gene CYP2C19 and acute myeloid leukemia.