The binding of Bcl-2 to IP3R2, which displays the highest sensitivity to its ligand IP3, and the concomitant suppression of IP3R2 activity may enable cancer cell survival in two ways: (i) by preventing the occurrence of excessive, pro-apoptotic Ca2+-release events and (ii) by establishing low-level Ca2+ signaling that drives the mitochondrial metabolism of cancer cells [39, 40]. The gene discussed is ITPR2; the disease is cancer.