Paradoxically, however, inactivation of DAP12 normalizes aberrant microglial signaling associated with AD pathology, ameliorates abnormal electrophysiological activity, and improves cognitive deficits in both amyloid and tauopathy mouse models [18–20], indicating that removal of DAP12 confers brain resilience in response to the toxicities of AD pathologies. This evidence concerns the gene TYROBP and amyloidosis.