Although data in the literature highlighted the similarities between post-COVID-19 syndrome and lung fibrosis, studies have reported the possible involvement of inflammatory cytokines, the renin–angiotensin system, the potential role of galectin-3, epithelial injuries in fibrosis, alveolar type 2 involvement, neutrophil extracellular traps, and other specific aspects (relationship with clinical and mechanical factors, epithelial transition mesenchymal, TGF-β signalling pathway, macrophages). This evidence concerns the gene TGFB1 and pulmonary fibrosis.