Supporting the protective and inhibitory role of Smad7 in tissue fibrosis and inflammation, the Smad7 deficiency observed in RA patients enhanced NF-κB signalling, Th1/Th17 differentiation, and synovial inflammation, probably through the hyperactivation of the TGF-β/Smad3-IL-6 molecular pathway, which is no longer controlled because of Smad7 inhibition [146]. Here, TGFB1 is linked to rheumatoid arthritis.