Anti-apoptotic Bcl-2 proteins regulates apoptosis by modulating the ER-mitochondrial Ca2+ transfer via the MAMs [65] while overexpression of pro-apoptotic Bcl-2 decreased both ER-Ca2+ release either by the direct control of IP3R3-mediated pore opening or by lowering the Ca2+ content of the ER, which weakens Ca2+-triggered MPT, and thus enables cancer cell to resist to apoptosis [66]. Here, BCL2 is linked to cancer.