A significant increase in miR-146a expression has also been reported in peripheral blood mononuclear cells and monocytes from rheumatoid arthritis patients, but no differences in the levels of TRAF6 and IRAK1 were shown between patients and controls, thus leading to the hypothesis that defective negative regulation of the target genes by miR-146a contributes to sustained pro-inflammatory cytokine production in patients18. This evidence concerns the gene TRAF6 and rheumatoid arthritis.