A possible role for Janus kinase (JAK)-inhibitors has been suggested from animal models of ILD associated with arthritis (208) as the JAK2 isoform specifically mediates TGF-beta signaling and the activation of myofibroblasts, and has been advocated in the molecular pathophysiology of RA-ILD (209, 210). This evidence concerns the gene JAK2 and rheumatoid arthritis.