GRIA2 and Neurodevelopmental delay: Functionally validated variants are so far best described for GRIA2 and GRIA3 for which more than 20 missense, insertion/deletion (indel) or stop-gain variants have been reported to change normal receptor function or disrupt or truncate subunit structure; strongly suggesting a linkage between specific GRIA2 and GRIA3 variants and NDD phenotypes.8