Overexpression of miR-21 promoted increases in the levels of proinflammatory markers and increased the amount of macrophage infiltration into diabetic kidneys, whereas knockdown of miR-21 can block the progression of renal fibrosis and inflammation, because suppression of miR-21 may inhibit the activation of the TGF-β and NF-κB signaling pathways [33, 39]. Here, TGFB1 is linked to renal fibrosis.