Interestingly, we found that the single agent of BKM120 was unable to significantly alter the expression level of c-Myc; however, the capability of BKM120 to reduce the survival rate of AML cells was potentiated upon c-Myc inhibition using 10058-F4, suggestive of the plausible contribution of c-Myc in leukemic cell response to the PI3K inhibitor. The gene discussed is MYC; the disease is acute myeloid leukemia.