Numerous prior studies have shown that selectively inhibiting mGluR5 or its downstream signaling normalizes protein synthesis and rescues a multitude of synaptic and behavioral phenotypes in Fmr1 KO.73 Similarly, enhancing mTORC1 signaling through the introduction of the Tsc2 mutation corrects synaptic pathophysiology in FXS.42 This motivated us to try to reverse the core pathophysiology associated with Fmr1 KO mice by increasing mNMDAR signaling through the introduction of GluN2A2BCTD mutation. The gene discussed is FMR1; the disease is fragile X syndrome.