Combined inhibition of CK1⍺, CDK7, and CDK9 resulted in a stabilization of p53 and β-catenin production, downregulation of Mdm2 and disrupted many SE responsible for the expression of several important oncogenes that included MYC, MYB, and MCL1 in MLL-AF9 induced and Tet2-/-Flt3ITD AML mice models [84]. This evidence concerns the gene KMT2A and acute myeloid leukemia.