Regarding the therapeutic targeting of the JAK/STAT signaling pathway, pharmacological inhibition of STAT3 was reported to prevent TGF-β-mediated myofibroblast formation in both experimental skin and lung fibrosis [43,116], while the selective JAK-2 blockade by the specific inhibitor TG101209 or by siRNA significantly reduced collagen synthesis in SSc fibroblasts and prevented fibrosis in two different SSc mouse models [189]. Here, STAT3 is linked to systemic sclerosis.