Overexpression of TIR8/SIGIRR in RA synovial cells led to a significant inhibition of spontaneous release of pro-inflammatory mediators, suggesting that either ILRs and/or TLRs signaling was at least partly responsible for the chronic production of those mediators in RA (Drexler et al., 2010). Here, IARS1 is linked to rheumatoid arthritis.