Treatment of AML cells with BTX-A51 robustly stabilizes and activates the p53 protein via a combined action of CK1α inhibition and shutdown of MDM2 expression, and at the same time it preferentially suppresses SE-driven transcription of key oncogenes such as MYC, MCL1, and MYB, enabling selective apoptosis of leukemic stem cells (20). The gene discussed is TP53; the disease is acute myeloid leukemia.