However, its persistent overexpression, as seen in keloids and hypertrophic scars,[52] likely due to high TGF‐β and IL‐1α signaling,[53] may contribute to dermal fibrosis, characterized by excessive α‐SMA‐positive (myo)fibroblasts, increased ECM deposition, and fibroblast hyperproliferation.[54, 55]. The gene discussed is IL1A; the disease is keloid.