Surprisingly, as opposed to its anti-inflammatory role in peripheral MΦs, SRC-2 drives neuroinflammation through activation of a proinflammatory program in microglia (MG) (87); conditional KO (cKO) of SRC-2 in myeloid cells significantly reduces experimental autoimmune encephalomyelitis (EAE) severity, which in part is associated with persistence of a homeostatic MG signature, rather than a pro-inflammatory profile and activity that are associated with SRC-2 deficiency in BM and WAT-resident MΦs (Figure 2A). Here, NCOA2 is linked to experimental autoimmune encephalomyelitis.