Karianan et al., in fact, indicate how disruption of the two distinct mechanisms of eCB inactivation, combining transport and FAAH inhibitors AM404 and AM374, causesadditive effects mediated by potentiation of eCB tone acting on CB1 receptors.Accordingly, by enhancing AEA availability, through inhibition of AMT and FAAH, most deficits (e.g. akinesia and sensorimotor orientation) were ameliorated in an experimental model of PD [54]. This evidence concerns the gene FAAH and Parkinson disease.