Thus, although TGFβ has emerged as a major disease modifier in RDEB and has provided a unifying mechanism for a range of independent studies identifying diverse routes to TGFβ activation [22,23,24,25,26], data do not identify a single, unifying mechanism of activation and likely points to a combination of contributing factors [22]. This evidence concerns the gene TGFB1 and recessive dystrophic epidermolysis bullosa.