Supporting this premise, small molecules co-targeting casein kinase 1A1 (CKIα) as well as CDK7 and P-TEFb have a striking therapeutic effect in pre-clinical models of acute myeloid leukemia, whereby inhibition of CKIα activates p53 while co-inhibition of CDK7 and P-TEFb synergizes in stimulating apoptosis (20). This evidence concerns the gene CSNK1A1 and acute myeloid leukemia.