Transforming growth factor-beta (TGF-β) which regulated p38 MAPK by hyperosmolarity, oxidative stress, and/or inflammatory cytokines to lead to the phosphorylation of downstream targets and activated the nuclear transcription factor-induced apoptosis response [49], showed differences in its protein abundance in podocytes and aortic endothelial cells of Fabry disease patients with nephropathy [50,51]. This evidence concerns the gene TGFB1 and kidney disorder.