In order to validate the predicted AML sensitivity to tivantinib, we treated HL60 and U937 AML cell lines with (−)-tivantinib, which is currently in advanced clinical development, its enantiomer (+)-tivantinib, which is a much weaker GSK3 inhibitor, the bona fide pan-GSK3α/β inhibitor LiCl and the MET inhibitor PF-04217903 as indicated. The gene discussed is MET; the disease is acute myeloid leukemia.