Lung fibrosis during the course of COVID-19 is directly associated with either the negative impact of the virus on alveolar epithelial cells or the promotion of the inflammatory response and induction of macrophages and monocytes, which release several inflammatory mediators like tumor growth factor beta (TGFβ), platelet-derived growth factor (PDGF), and soluble CD163 (sCD163). This evidence concerns the gene TGFB1 and pulmonary fibrosis.