Increased expression of FGFR1, FGFR2, CTGF, and TGF-β1 in the ducts of the sweat glands indicates a potential role for them in the pathogenesis of DD, which is in contrast to a previous study which suggested that only secretory portions contribute to profibrotic signaling [18]. This evidence concerns the gene TGFB1 and dentin dysplasia.