Thus, the mechanisms for the pathological deposition of ECM in keloids are partially related to the proliferation of mesenchymal fibroblasts, which is possibly driven by fibrogenic growth factors, including transforming growth factor (TGF)-β, fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), and POSTN [13,16,17]. The gene discussed is VEGFA; the disease is keloid.