Thus, strategies to avoid these deleterious effects could involve inhibiting TGF-β signaling selectively in excessive activated lung fibroblasts, as TGF-β-triggered Smad2/3 signaling is pivotal in the induction of pulmonary fibrosis in animal models (Figure 6) (Aschner et al., 2020). The gene discussed is TGFB1; the disease is pulmonary fibrosis.