Whether this may have relevance for the distinct clinical therapeutic/side effect profile of clozapine remains to be investigated but it is worth noting that the inverse agonism of Gαq by clozapine through the 5-HT2AR was found to potentiate Gαi signaling through the 5-HT2AR-mGlu2R heterocomplex that is upregulated in schizophrenia, and to be involved in the mechanism of its antipsychotic activity [12, 54]. This evidence concerns the gene GNAQ and schizophrenia.