The hypothesis of an involvement of IL-23 in the pathogenesis of RA-ILD exerted by promoting mTOR/S6 signaling-dependent EMT in alveolar epithelial cells was supported by transcriptional sequencing analysis of human lung fibrosis biopsy tissue [63], which detected a significant increase in IL-23 mRNA expression in RA-ILD lung sections positively correlated with transitioning ATI epithelial cell [63] (Figure 3). Here, IL23A is linked to rheumatoid arthritis.