DDIT3 and cancer: Maintaining redox homeostasis is a delicate balance since although high ROS levels are cytotoxic because of oxidative stress, cancer cells also derive benefits from sustaining higher than normal levels of ROS which promotes by activation of pro‐oncogenic signaling pathways.[55] Instructively, reductions in ROS resulting from decreased OXPHOS activity can inhibit cancer cell growth.[56] In this respect, the mitochondria‐localized pool of DDIT3 makes a significant impact in moderating the temporal ROS responses during glutamine deprivation.