Congenital disorders of glycosylation (CDGs) are a broad span of metabolic disorders. Glycosylation generally has two types, which are N-linked and O-linked. Disorders of O-linked glycosylation present clinically as autism, epilepsy, and facial dysmorphia. We study mouse models of GALNT2 neuronal knockout, which affects the first step of the O-GalNAc glycosylation type. Glycoproteomics data analysis allows us to narrow down to two candidate substrate proteins that are most significantly affected by the loss of the GalNAc transferase 2 enzyme–measured by glycan truncation, the substrate protein’s relationship with expected CDG symptoms, and the predicted contribution of other GalNAc-T family members to glycosylation at a specific site.