It has already been shown that in experimental autoimmune encephalomyelitis and experimental stroke, microglia-specific TAK1 KO mice showed neuroprotective effects and strongly diminished CNS inflammatory responses including abolished activation of NF-κB and reduced expression or release of inflammatory cytokines (such as IL-1β and TNF-α) and chemokines (such as CCL2) [20, 34]. The gene discussed is CCL2; the disease is experimental autoimmune encephalomyelitis.