Furthermore, studies using the 5xFAD mouse model show that INPP5D/SHIP1 is upregulated as Aβ pathology progresses and that INPP5D/SHIP1 haploinsufficiency normalizes AD‐related neuropathology and behavioral deficits, which suggests that inhibition of INPP5D/SHIP1 early in AD would increase TREM2 signaling and microglial protective functions, resulting in reduced rate of disease progression and cognitive decline in AD.112. Here, TREM2 is linked to Alzheimer disease.