scRNA‐seq also revealed that TEM1 (CD248), a transmembrane protein enriched in scar fibroblasts, enhances TGF‐β signaling via receptor stabilization; its knockdown reduces ECM production in vivo, and therapeutic blockade via ontuxizumab has been shown to be effective in suppressing keloid growth [116]. The gene discussed is TGFB1; the disease is keloid.