Given that we have previously demonstrated that elevations of FAAH within the amygdala following the induction of colitis were associated with the development of anxiety (Vecchiarelli et al., 2021), which in peripheral inflammatory contexts is known to be driven by inflammatory cytokines within the amygdala proper (Chen et al., 2013), these data also suggest that a potential mechanism by which elevated AEA signaling may be able to dampen inflammation-associated anxiety is via a suppression of inflammatory cytokine levels within the amygdala. Here, FAAH is linked to colitis.