Xu et al. observed iron deposition, lipid radical accumulation, and mitochondrial shrinkage in a mouse model of ulcerative colitis (UC), and also found that the PERK–ATF4–CHOP pathway was significantly activated in the colonic epithelium of UC mice, and that treatment with GSK414, an inhibitor of the ER stress PERK pathway, significantly inhibited the process of ferroptosis [25]. The gene discussed is ATF4; the disease is ulcerative colitis.