These results were validated in vitro, demonstrating that AML differentiation was associated, in addition to induction of CD11b, with down-regulation of MYC (Fig. 2E and Supplementary Fig. 2E), an increase in the cell-cycle inhibitors CDKN2A (p21) and CDKN1A (p16) (Fig. 2E and Supplementary Fig. 2E) together with cell-cycle arrest (Fig. 2F and Supplementary Fig. 2F). The gene discussed is CDKN2A; the disease is acute myeloid leukemia.