As an immune receptor almost exclusively expressed in microglia and myeloid cell types, mutational variants in TREM2 such as the rare R47H mutation has been shown to significantly increase risk of AD onset [22, 34], where TREM2 R47H has been shown to alter Aβ plaque morphology, microglial energy metabolism, and impaired binding to TREM2 ligands such as APOE and Aβ oligomers [3, 60, 65–67]. The gene discussed is APOE; the disease is Alzheimer disease.