This observation led to propose that the antipsychotic activity of mGlu2/3 agonists could in part rely on their ability to functionally antagonize the colocalized 5-HT2A receptors and, conversely, that pathological alterations of the mGlu2/3–5-HT2A receptor–receptor coupling could account for developing schizophrenia (Marek et al., 2001; González-Maeso et al., 2008; Moreno et al., 2016). The gene discussed is GRM2; the disease is schizophrenia.