Microglia A20 deficiency exacerbated multiple sclerosis (MS)-like disease, due to hyperactivation of the NLRP3 inflammasome leading to increased interleukin-1β secretion in mice, suggesting that A20 critically controls microglia activation and inhibits inflammasome-dependent neuroinflammation [43]. This evidence concerns the gene TNFAIP3 and multiple sclerosis.