Previous studies have found the phosphorylation of RBM17 regulated by mitogen-activated protein kinase (MAPK)42 and Cdc2-like kinase 1(Clk1)51 affects its alternative splicing site utilization highlighting the possibility that selective small molecule Clk inhibitors52,53 may offer a strategy for targeted RBM17 interference as an AML therapy. This evidence concerns the gene CLK1 and acute myeloid leukemia.