The discovery that BH3-only proteins are critical for the initiation of apoptosis triggered by diverse anti-cancer agents, and that genetic deletion of distinct pro-survival BCL-2 proteins can effectively kill certain types of malignant cells, gave rise to the concept that pharmacological inhibitors of pro-survival BCL-2 proteins that mimic the function of BH3-only proteins could be effective in cancer therapy [20, 21]. The gene discussed is BCL2; the disease is cancer.