This mediator, which showed a remarkable protective effect against glutamate-induced cytotoxicity and oxidative stress, and markedly suppressed the glutamate-induced activation of ERK in the late phase, is a dual antagonist of FAAH and TRPV1 [64, 65], and was also tested in an in vivo model of Parkinson’s disease to investigate its effects on L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID), which is a common side effect of the long-term treatment with L-DOPA. Here, FAAH is linked to Parkinson disease.