Inhibition of AREG or EGFR in TGF-β1-stimulated lung fibroblasts diminished AREG-dependent fibroblast proliferation, expression of α-smooth muscle actin and collagen [186], strongly suggesting a role of EGFR/ADAM17/AREG signaling in pulmonary fibrosis in vivo. The gene discussed is EGFR; the disease is pulmonary fibrosis.