Our results demonstrating increased ERK phosphorylation at Thr202 and Tyr204 (a marker of MEK activation) residues in Kasumi-1 cells, without AKT activation, are supported by earlier findings of higher ERK activity in Kasumi-1 cells compared to other AML cells, with no significant phosphorylation of Ser473 of AKT32. The gene discussed is AKT1; the disease is acute myeloid leukemia.