They show that STAT3 is activated by various kinases, including JAK, Src, c-ABL, and JNK, in response to TGF-β stimulation and that genetic and biochemical blockade of STAT3 activity prevented TGF-β-induced fibroblast-to-myofibroblast transition and mitigated skin fibrosis in two mouse models of scleroderma [195]. The gene discussed is STAT3; the disease is scleroderma.