MaR1 promoted inflammation resolution by inhibiting chemotaxis, TNFα, IL1β, IL18 levels and NLRP3 inflammasome or NF-kB activation and regulating microglia activation in rodent models of Alzheimer’s disease [85], non-compressive lumbar disc herniation [86] or inflammatory pain [87]. This evidence concerns the gene NFKB1 and lumbar disc herniation.