TGFB1 and COVID-19: Moreover, COVID-19 patients presented high levels of: (1) INF-γ, known for increasing the Th1 response and a profibrotic inflammatory profile [38,46]; (2) TGF-β, which enhances the recruitment of fibroblasts with the subsequent differentiation in myofibroblasts [38]; (3) IL-17, which stimulates neutrophil degranulation and oxidative stress damage, both involved in the development of fibrosis [47] (Figure 2).