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A typical example of this potential problem might be represented by the failure, to date, of FAAH inhibitors to counteract inflammatory and chronic pain in clinical trials, when the fact that such molecules elevate the levels not only of AEA but also of N -palmitoylethanolamine and N -oleoylethanolamine, which may consequently act at targets such as TRPV1 and GPR55, may explain the lack of efficacy
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