BCL2 and neoplasm: In this scenario, A398 showed low cytotoxicity against normal cells and was cytotoxic to several human tumor cell lines, inducing apoptosis in the leukemic HL-60 cells through the activation of the extrinsic and intrinsic pathways of death and acting on molecular targets that are amenable to therapeutic intervention, such as caspases, the anti-apoptotic protein Bcl-2 and MAPKs (as indicated in the graphical abstract, Figure 5).