miR-146a/b and miR-155 are of particular interest for inflammatory signalling to NF-κB, since these miRNAs can be induced by inflammatory stimuli such as IL-1β, TNF and TLRs [78,79]. In addition, miR-146a is an NF-κB-dependent gene, and the NF-κB signalling molecules IRAK1 and TRAF6 were identified as target genes of miR-146a [78] (Figure 1). Similarly, miR-155 was shown to target transcripts for the NF-κB signalling molecules IKKε and RIP1 [79,80]. Notably, both miR-146 and miR-155 are expressed at higher levels in RA synovial fibroblasts and synovial tissue [81,82], as well as in peripheral blood mononuclear cells of RA patients [83]. miR-146a is also overexpressed in CD4+ and IL-17-producing T cells from RA patients [84,85]. Interestingly, a polymorphism in the 3'-UTR of the miR-146a target gene was recently shown to be associated with RA susceptibility [86]. miR-155 overexpression in synovial fibroblasts was able to prevent the TLR and cytokine-inducible expression of specific matrix metalloproteinases that mediate tissue destruction in RA [81]. Moreover, miR-155 was shown to promote TNF production, a key process in the pathogenesis of RA [87]. miR-146 and miR-155 may therefore be important negative regulators of inflammation in RA and their potential for the development of new treatments is substantial. In addition, their increased expression in RA patients is potentially useful as a marker for disease diagnosis, progression, or treatment efficacy [88], but this will require confirmation using a large and well-defined cohort.