New risk loci have been identified in genome-wide association studies (GWAS) and implicated in different pathways of AD, such as synaptic function (BIN1, CD2AP, SORL1, EPHA1, and PICALM), cholesterol metabolism (ABCA7, CLU and SORL1), and immune response (CD33, ABCA7, MS4A, EPHA1, CLU and CR1) [8,9,10,11]. This evidence concerns the gene EPHA1 and Alzheimer disease.