This seems to block TGF-β—that inhibits the expression of the receptor and the nuclear translocation of SMAD2/3—which in turn alters the expression of collagen [49] as well as of the IGF-1 signal, through the reduction in the receptor and intracellular signaling, thus influencing the proliferation of keloid fibroblasts and reduces the contraction of collagen [50]. The gene discussed is IGF1; the disease is keloid.