A rationale for implicating inflammatory diseases in AD etiology has been provided by genomic studies showing associations between AD and polymorphisms in a number of genes involved in immune cell function, such as Apolipoprotein E (APOE), Triggering receptor expressed on myeloid cells 2 (TREM2), CD33 (Jonsson et al. 2013; Guerreiro et al. 2013; Griciuc et al. 2013). This evidence concerns the gene CD33 and Alzheimer disease.