Notably, MCU, whose conductivity for Ca2+ is positively regulated by ROS-driven S-glutathionylation [35], also controls cell-cycle progression by generating spontaneous mitochondrial Ca2+ transients that coordinate mitotic entry supporting proliferation [36,37], thus suggesting yet another mechanism for ROS-driven alterations in mitochondrial Ca2+ fluxes to support tumor progression. Here, MCU is linked to neoplasm.