Estrogen clearly augments the development of lung fibrosis (Figure 4); yet, the binding of ERα to the STAT3 promoter shifts profibrotic cytokine expression away from proinflammatory phenotypes mediated by IL-17A to immunosuppressive phenotypes mediated by TGF-β1 (Figure 2 and Figure 3). The gene discussed is STAT3; the disease is pulmonary fibrosis.