In addition to Aβ and tau pathologies, dysfunctional microglial response has been postulated as a driver for AD onset and development, especially since the identification by GWAS of several genetic AD-risk factors related to microglial functions (such as CR1, CLU, MEF2C, EPHA1, TREM2, CD33, ABCA7 and MS4A), which constituted a decisive turning point in AD research [207]. Here, CD33 is linked to Alzheimer disease.