In in vivo experiments using PDX mouse model, a CDK inhibitor dinaciclib which inhibits CDK5-mediated RalGEF signaling induced leukemic cell apoptosis and prevented evolution of NRI-AML, suggesting that RalGEF signaling is involved in escaping mechanism of RAS-mutated AML and can be a potential therapeutic target. This evidence concerns the gene CDK5 and acute myeloid leukemia.