Since many studies have shown loss‐of‐function or decrease in TREM2 expression in AD,[15] both sporadic (CRISPR‐Cas9‐based APOE4 lines; validation with iPSC‐derived astrocytes in Figure6a) and familial (APPNL‐G‐F/MAPT dKI mice) AD models were used for validating TREM2‐dependent defect in microglial phagocytosis. Here, TREM2 is linked to Alzheimer disease.