Nevertheless, aberrant expression of various TGF-β signalling components have been previously shown to trigger this 'synthetic' myofibroblast phenotype in other fibro-proliferative disorders, specifically keloids and burn hypertrophic scarring [34,44,45], that can to some extent be inhibited by neutralizing anti-TGF-β2 antibodies [46,47]. This evidence concerns the gene TGFB2 and keloid.