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. Here, ACSF2 is linked to ulcerative colitis.