Indeed, an anti-survival role was highlighted in breast and colon cancer, where TRPM2 activation by chemotherapy agents resulted in Ca2+ entry, intracellular Ca2+ overload, and increased mitochondrial depolarisation, leading to cell death [153], and in prostate cancer, where H2O2-induced TRPM2 activation resulted in PC3 cells’ death via Ca2+-dependent inhibition of autophagy [102] (Figure 1). The gene discussed is TRPM2; the disease is prostate cancer.