Inhibition by negative allosteric modulator (NAM) of mGluR5 corrects hyperactivity, seizures and elevated synaptic protein synthesis in Tsc2 mutant mice, whereas positive allosteric modulation of mGluR5 results in the exacerbation of hyperactivity and epileptic phenotypes, suggesting a meaningful therapeutic potential for mGluR5 NAM in TSC (Kelly et al., 2018). This evidence concerns the gene GRM5 and tuberous sclerosis.