By attacking multiple kinases including FLT3, PIM1, AURK, and AKT, whose functions are not fully overlapping but all essential for FLT3-ITD- and/or FLT3-TKD-dependent AML growth and survival, CDK6 inhibition may reduce the chances of acquisition of FLT3 resistance mutations and lead to more durable clinical response [26,27]. The gene discussed is CDK6; the disease is acute myeloid leukemia.