In light of the ability of canonical Wnt pathway to stimulate fibroblast activation and mesenchymal progenitor cell differentiation [28,30], and the association of transgenic Wnt10b expression with scleroderma-like skin fibrosis and subcutaneous lipoatrophy in the mouse [31], hyperactivation of canonical Wnt signaling in SSc skin biopsies, while suppressing adipogenesis, aberrant Wnt signaling is likely to be important in the pathogenesis of SSc, and is an interesting potential target for therapy. The gene discussed is WNT10B; the disease is systemic sclerosis.