TREM2 and PLCγ2 function has until recently been more thoroughly investigated in peripheral immune cells than in the CNS, with variants of these genes known to cause diseases such as Nasu-Hakola disease (TREM2) [22], and PLCγ2-associated antibody deficiency (PLAID), or autoinflammation and PLAID (APLAID) [3]. The gene discussed is TREM2; the disease is autoinflammation-PLCG2-associated antibody deficiency-immune dysregulation.