TGFB1 and systemic sclerosis: Previously, the TGFβ pathway, Toll-like receptor signaling, and the WNT pathway were reported to be the main dysfunctional signaling pathways in the skin of patients with SSc [47], and the TGFβ and Wnt/β-catenin pathways have been found to be hyperactivated to promote ECM production and induce fibrosis [48, 49].