Keloids result from dysregulation in the proliferation and remodeling phases, leading to abnormal ECM accumulation and scarring; hyperactive fibroblasts, stimulated by elevated levels of TGF-β1 and VEGF, drive excessive collagen synthesis—particularly types I and III—while reduced ECM degradation due to altered MMP activity and increased TIMPs promotes fibrotic tissue extending beyond the wound margin (37, 38), highlighting the complexity of keloid formation and its clinical challenges. This evidence concerns the gene VEGFA and keloid.