However the precise regulatory mechanisms underlying the paradoxical dual roles of Tregs in fibrosis particularly the critical tipping points that determine their pro-fibrotic versus anti-fibrotic functions remain poorly understood and represent a significant knowledge gap in keloid pathogenesis future research should prioritize single-cell analyses to dissect Treg heterogeneity in keloid niches and investigate how microenvironmental cues such as chronic TGF-β exposure or metabolic reprogramming bias Tregs toward pathogenic phenotypes. The gene discussed is TGFB1; the disease is keloid.