Given its central role, therapeutic strategies targeting TGF-β activation and signaling pathways have been actively developed.10 However, owing to the widespread involvement of TGF-β in essential physiological processes, directly targeting TGF-β in IPF presents significant challenges.11,12 Many clinical trials have been halted because of severe side effects and insufficient inhibition of TGF-β signaling.13–15 Therefore, the most ideal therapeutic approach would selectively inhibit excessive TGF-β induced by pulmonary fibrosis, while preserving the basal TGF-β levels crucial for homeostasis. The gene discussed is TGFB1; the disease is idiopathic pulmonary fibrosis.