We propose that SAV containing ART631 (or potentially other 2C-ARTs) offers a good starting point for a future novel, low-toxicity treatment paradigm for AML that can potentially be improved upon with either additional synergistic agents or with substitutions for either SOR or VEN; namely, with more potent and selective kinase and BCL2 inhibitors, respectively (26–29). The gene discussed is BCL2; the disease is acute myeloid leukemia.