A possible mechanism has been proposed: decreased miR-363 expression in DCs from RA patients was shown to upregulate the expression of integrin av, which induced the activation of TGF-β and promoted the differentiation of Th17 cells (29); Th17 cells can exacerbate RA and are directly involved in cartilage and bone destruction (83). This evidence concerns the gene TGFB1 and rheumatoid arthritis.