The overexpression of Cnr1 in Shank3∆11/∆11 mice might therefore result from a compensatory upregulation in response to the alterations of the endocannabinoid system which has been previously reported in SHANK3-deficient mice (Wang et al., 2017; Folkes et al., 2020), in valproic acid induced rat models of autism and also in some autistic individuals (Zou et al., 2021). The gene discussed is CNR1; the disease is autism.