Variant class and intellectual outcome show a significant correlation: heterozygotes for a grin2b pathogenic variant resulting in a null allele (e.g., nonsense or frameshift variants, deletion involving whole exons or the entire gene, translocation and inversion disrupting grin2b) tended to display mild or moderate intellectual disability (ID), while heterozygotes for pathogenic missense variants displayed severe ID (Fisher's exact test, p=0.0079) [5], which explains a moderate clinical picture in our patient. The gene discussed is GRIN2B; the disease is Intellectual disability.