Lung fibrosis following COVID-19 develops due to a complex disruption of homeostasis, involving inflammation, oxidative stress, coagulation abnormalities, chemoattractant mediators and key cytokines, such as TGF-β1 (transforming growth factor beta 1), PDGF (platelet-derived growth factor), IL (interleukin)-6, IL-11, and IL-17, which collectively drive the proinflammatory and profibrotic processes [7,8]. The gene discussed is IL6; the disease is pulmonary fibrosis.