Efforts to target TGFβ as a therapeutic strategy to reduce SSc lung fibrosis have not been effective, and concerns about potential adverse complications due to the pleiotropic roles of TGFβ in lung physiology have led to efforts focusing on targeting other pro-fibrotic factors and molecular pathways as a therapeutic strategy to treat SSc [1,30,31]. Here, TGFB1 is linked to systemic sclerosis.