The coronavirus has a role in fibrosis both for continuous tissue injuries mediated by persistent viral–ACE2 receptor interaction leading to abnormal and irregular healing, and for the release of profibrotic factors, like transforming growth factor β (TGF-β), tumor necrosis factor α (TNF-α), insulin-like growth factor-1 (IGF-1), platelet-derived growth factor (PDGF), connective tissue growth factor (CTGF), and extracellular matrix deposition which collectively activate lung fibroblasts and start pulmonary fibrosis. This evidence concerns the gene TNF and pulmonary fibrosis.