Because our experiments revealed that TGF-β protein and several internal signaling molecules such as phosphor-Smad 2/3 complex, Erk 1/2, Akt, and NF-κb are overexpressed by HMGB1 in HDFs and normal tissues, modulating HMGB1 expression or its signaling is a potential therapeutic approach for preventing or inhibiting dermal fibrosis and keloid formation. The gene discussed is TGFB1; the disease is keloid.