Decreased NMDA receptor function is a central mechanism implicated in various brain disorders, and extensive efforts to modulate NMDAR activity have been devoted in various therapeutic settings. We have previously established Slc6a20a as a novel glycine transporter, and using an antisense oligonucleotide ASO against Slc6a20a, we sought to modulate NMDAR function in well-established models of psychiatric disorders Shank2 and Shank3 mutant mice.