MiR-19a/b can act as a negative regulator of the inflammatory response in RA-FLSs, which is supported by evidence showing that miR-19a/b diminishes IL-6 and MMP-3 production via direct control of TLR2 expression.102 MiR-27a inhibition in RA-FLSs significantly promotes cell migration and invasion by targeting the 3′ UTR of follistatin-like protein 1 (FSTL1) and further interfering with TLR4/NF-κB signaling.103 STAT3 and caveolin 1 (CAV1) have been identified as direct targets of miR-29a and miR-192 in RA-FLSs, respectively. This evidence concerns the gene TLR4 and rheumatoid arthritis.