Several studies have suggested that BV6 can act in concert with a series of commonly used clinical drugs in AML treatment, such as cytarabine, the demethylating agents azacitidine or decitabine and the histone deacetylase inhibitors MS275 or SAHA, to trigger necroptosis in apoptosis-resistant AML cells in a synergistic manner mediated by TNFα/RIPK1/RIPK3/MLKL activation [125–127]. The gene discussed is MLKL; the disease is acute myeloid leukemia.