In parallel, efforts to characterize the molecular architecture of HTS and keloids have revealed a dense network of interlinked signaling pathways—TGF‐β, Wnt/β‐catenin, YAP/TAZ, JAK/STAT, and Notch—each contributing to fibroblast activation, immune modulation, and matrix remodeling [195]. The gene discussed is TGFB1; the disease is keloid.