In the process of IPF, mitochondria activate the TGFβ1 pathway after excessive stress during oxidative stress, and NOX4 is overexpressed in NADPH oxidase, which further promotes the process of pulmonary fibrosis [20–23], which may be one of the most critical processes in the process of IPF, which may be effectively reversed by MitoQ. Here, FMO5 is linked to idiopathic pulmonary fibrosis.