However, sustained activation of mTORC1 can lead to pulmonary fibrosis (Gui et al., 2015) and drive neuromuscular junction structural alterations, resulting in myofiber denervation (Ang et al., 2022), muscle atrophy, loss of muscle mass (Tang et al., 2014, 2019) and late-onset myopathy by increasing the expression of the E3 ubiquitin ligases atrogin1 and MuRF1 and impairing autophagy (Castets et al., 2013). This evidence concerns the gene FBXO32 and pulmonary fibrosis.