ILC2s are regulated by a large range of tissue signals, including prostaglandins, neuropeptides, metabolic cues, and alarmins such as IL‐25, IL‐33, and IL‐18 released by damaged epithelial cells.[7] Upon intestine injury, IL‐33 released by necrotic cells promotes ILC2s accumulation and type 2 cytokines secretion, concomitant with amphiregulin (Areg) production, to elevate tissue repair by enhancing epithelial cell proliferation, stem cell renewal and mucin production by goblet cells in DSS colitis.[8, 9, 10, 11]. This evidence concerns the gene AREG and colitis.