On the other hand, in the study by Aguilar et al. (2018), pubertal exposure to WIN55212 or to the fatty acid amide hydrolase (FAAH) inhibitor URB597, which increases endogenous anandamide levels, augmented the proportion of second-generation MAM rats that develop schizophrenia-like deficits. Here, FAAH is linked to schizophrenia.