The UPR has a critical role in cancer cell death and homeostasis regulation, and pharmacological agents that activate the UPR can induce cell death by increasing the levels of apoptosis‐inducing proteins, such as CHOP and ATF6.[42] During the UPR, ATF6 is released from the ER and subsequently transported to the Golgi, where it is cleaved by S1P and S2P. The gene discussed is DDIT3; the disease is cancer.