On the other hand, cancer cells frequently activate the UPR to adapt and modulate anti-apoptotic signals, gaining the ability for self-selection and survival in unfavorable environments; the activation of PERK via ARE, Keap1, and ATF4 promotes survival in conditions of nutrient deficiency, ATP shortage, ROS production, and hypoxia, while the modulation of IRE1α induces the expression of XBP1, XBP1, and ERAD, aiding in the survival of malignant cells7. This evidence concerns the gene ERN1 and cancer.