FOXO3 directly bound to SPON1 and its promoter, promoted the formation of SPON1 circRNA, inhibited the nuclear translocation of Smad3 through interaction with Smad3 and sponge Smad7 as the targeted miRNAs to promote Smad7 expression, and ultimately inhibited the progression of pulmonary fibrosis (Figure 7). The gene discussed is SPON1; the disease is pulmonary fibrosis.