Although once viewed as a downstream consequence of AD pathogenesis, genome-wide association studies have implicated innate immunity as causative in the disease process, with variants of microglial regulators identified as key AD risk factors such as triggering receptor myeloid 2 (TREM2) and its downstream signaling molecule, Src homology 2 (SH2) domain containing inositol polyphosphate 5-phosphatase 1 (SHIP1) (4–8). This evidence concerns the gene TREM2 and Alzheimer disease.