Mouse autism models based on gene knockouts that impact glutamatergic activity (and on prenatal valproic acid effects), show increases in NMDA and/or mGlur5 activity that are reduced by antagonists and negative allosteric modulators, with consequent reductions in social deficits, repetitive behavior or both; such effects have been demonstrated for the genes ADCY5 [186], EiF4ebp2 [187], FMR1 [188], IRSp53 [189], Shank2 [190], TSC1 [191], as well as for 16p11.2 deletions [192] and prenatal valproate [193]. The gene discussed is BAIAP2; the disease is autism.