Consistent with these results, several genetic mice models of ASD and ASD-related developmental disabilities all exhibit hypofunction of GluN2B (Peça et al., 2011; Li et al., 2015; Toft et al., 2016), suggesting the deficit of GluN2B function as a common postsynaptic mechanism that is associated with multiple neurodevelopmental diseases. This evidence concerns the gene GRIN2B and developmental disability.