Together, we have provided strong evidence demonstrating that in both TGFβ-activated normal lung fibroblasts and IPF fibroblasts, paracrine SPARC signaling not only dysregulates the alveolar epithelial barrier integrity,80 but also activates EGFR/RAS/ERK signaling in ATII cells to maintain a chronic wound-healing phenotype. The gene discussed is TGFB1; the disease is idiopathic pulmonary fibrosis.