Further examination of mNMDAR signaling revealed that spine shrinkage was dependent on the activation of mammalian target of rapamycin complex 1 (mTORC1) and new protein synthesis.24 Dysregulated synaptic protein synthesis and altered spine structure are features of fragile X syndrome (FXS), an NDD characterized by ID and ASD and caused by loss of the fragile X messenger ribonucleoprotein (FMRP).26–28 This structural readout of mNMDAR function was investigated in the mouse model of FXS, whereby the magnitude of spine shrinkage in response to NMDA appeared intact. The gene discussed is FMR1; the disease is Neurodevelopmental delay.