Inflammatory bowel diseases (IBD) are increasingly recognized as disorders in which ep-ithelial dysfunction and maladaptive regeneration are as important as immune dysregula-tion. Tumor necrosis factor (TNF), a key mediator of intestinal inflammation and a thera-peutic target, plays a dual role in both immune activation and epithelial repair by regulat-ing progenitor cell expansion, lineage plasticity, and chemokine signaling. During acute injury, TNF-driven responses are adaptive, promoting cry