A similar approach was used by Rahmani, et al. [65], which demonstrated the cooperation between the selective Bcl-2 inhibitor and PI3K inhibition (venetoclax/GDC-0980) in inducing Bax-dependent apoptosis, which exhibiting strong anti-AML activity both in vitro and in vivo, as well as against multiple forms of venetoclax resistance. This evidence concerns the gene BAX and acute myeloid leukemia.