Studies have shown that it triggers the disease by being poorly regulated. Therefore, antibodies against them have been developed, such as anti-TGF-β1 and anti-TGF-β2, which suppress the synthesis of collagen from keloid fibroblast cultures and human keloid derived xenograft collagen, demonstrating its role in the mechanism of the disease [4]. This evidence concerns the gene TGFB2 and keloid.