Although what might precipitate high AEA levels in patients who do not use cannabis is unclear,11 stress exposure, a key risk factor for schizophrenia,53 increases AEA levels54 and decreases CB1R density in the hippocampus.55 After illness onset, the experience of hallucinations and delusions may also increase stress levels56 and, in turn, the production of AEA,54 exacerbating reductions in CB1R levels.55 However, studies are needed to investigate whether stress may precipitate AEA and CB1R alterations in humans. This evidence concerns the gene CNR1 and Delusion.