Our rodent experiments suggest that inhibiting FAAH, via AM3506 administration, facilitates extinction by augmenting endogenous anandamide signaling in the amygdala. By extension, this raises the possibility that genetic variation in endogenous anandamide levels could affect fear-circuit function and predisposition to fear-related disorders in humans. Thus, based on our preclinical data we generated the a priori hypothesis that human fear-related endophenotypes associate with a common functional FAAH gene variant (C385A; rs324420) that produces reduced FAAH expression in lymphocytes.43