Corticosteroids, particularly intralesional TAC, are widely regarded as first‐line treatments for HTS and keloids because of their ability to inhibit fibroblast proliferation by suppressing the MAPK and PI3K/Akt pathways, inducing apoptosis via caspase‐3 activation and Bcl‐2/Bax modulation, and attenuating TGF‐β1/Smad2/3 signaling. The gene discussed is SMAD2; the disease is keloid.