Other studies based on other possible therapeutic targets suggest the use of regulating AD monocytes/macrophages and the role of fatty acid amide hydrolase [18]. This study was based on the analysis of the endocannabinoid (eCB) system, and the measure of elements of such system concluding that by decreasing the production of pro-inflammatory cytokines like TNF-, IL6, and IL-12 and increasing the production of the anti-inflammatory cytokine IL-10 in monocytes and monocyte-derived macrophages from AD patients, pharmacological FAAH inactivation was able to modulate their immune response [18]. The gene discussed is IL10; the disease is Alzheimer disease.