Within the IL23-IL17 axis, Zhang and colleagues reported that lung fibroblasts from patients with RA-ILD express significantly higher levels of the IL-17A receptor (IL-17RA) compared to patients without ILD or IPF (120) while IL-23 contributes to the epithelial-mesenchymal transition in the lung of RA-ILD (121). This evidence concerns the gene IL17RA and idiopathic pulmonary fibrosis.