Although this requires validation in a larger cohort of AD patients and further experiments are needed to better understand the molecular mechanism of such an immunological switch, perhaps due to an increase in CB2 expression or activation of specific transcriptional pathways, our findings suggest that FAAH might also be an ideal target for other neuroinflammatory and neurodegenerative diseases where innate immune cells are strongly implicated in their immunopathogenesis, such as multiple sclerosis and Parkinson’s disease. The gene discussed is CNR2; the disease is Alzheimer disease.