Although fibroblasts are major sources and targets of TGF-β, some fibrogenic transformations reflect the activation of other cell types such as macrophages and epithelial cells [13]; in addition, the promotion of TGF-β-dependent fibrosis in autoimmune diseases involves the activation of diverse mechanisms that will be clarified in the next paragraphs. This evidence concerns the gene TGFB1 and autoimmune disease.