Genetic or pharmacological inhibition of either IP3R or MCU elicits comparable effects to those observed in normal cells, including diminished OXPHOS, AMPK activation, and induction of a pro-survival autophagy (Figures 1B,C); however, whereas normal cells were able to survive these challenges, much of the cancer cell population (60–70%) could not (Figure 1C). The gene discussed is ITPR1; the disease is cancer.