Increasing evidence indicate that the activation of CB1 and CB2 receptors, by natural or synthetic agonists, mediates neuroprotective effects in in vitro and in vivo models of AD, reducing the deleterious effects of βA peptide or tau hyperphosphorylation (Esposito et al. 2007; Martin-Moreno et al. 2011; Janefjord et al. 2014; Ahmed et al. 2015). The gene discussed is CNR1; the disease is Alzheimer disease.