Our lab showed that VTN triggered NLRP3 inflammasomes activation, leading to trigger pyroptosis to aggravate inflammation in THP-1-derived macrophages [41], and in the current study, we further showed the potent pro-IBD effect of VTN originated in its ability to decrease SLC7A11 and GPX4 expression to induce ferroptosis, which leading to inhibit CDX2-mediated cell differentiation during mucosal healing. Here, GPX4 is linked to inflammatory bowel disease.