In our study, we demonstrated that DHEA not only inhibited G1 phase of cell cycle but also induced apoptosis through the activation of PERK-ATF4-CHOP axis under ER stress induction at 48 h after DHEA treatment in both wild-type and mutant p53 CRC cells (Figures 2–6). The gene discussed is ATF4; the disease is colorectal carcinoma.