ACSL4 has been shown to actively promote ferroptosis, evidenced by notable increases in lipid peroxidation, Fe2+ concentration, and ACSL4 expression in inflammatory models [45,46], Conversely, down-regulation of ACSL4 expression effectively mitigates ferroptosis, offering novel therapeutic avenues for ulcerative colitis treatment [47], Moreover, investigations led by Luo and colleagues at the University of California uncovered suppressed ACSF2 expression in animal models of Salmonella typhimurium colitis and cell models. The gene discussed is ACSL4; the disease is ulcerative colitis.