In gouty arthritis, Lian and colleagues elucidated that circHIPK3 was enriched in mononuclear cells of synovial fluid, which strikingly repressed miR-561 and miR-192, and thereby facilitated pro-inflammatory functions of toll-like receptor 4 (TLR4) and NLR family pyrin domain containing 3 (NLRP3) [116]. Here, TLR4 is linked to gout.