ALG13 encodes a subunit of the UDP-N-acetylglucosamine (UDP-GlcNAc) transferase enzyme complex, functioning as a key component in the N-linked glycosylation pathway within the endoplasmic reticulum 1. This pathway catalyzes the attachment of carbohydrate structures to asparagine residues in proteins, with N-glycosylated products participating in critical neurobiological processes including electrical gradient formation and neurotransmission 1. ALG13 mutations cause ALG13-Congenital Disorder of Glycosylation (ALG13-CDG), a rare X-linked disorder of N-linked glycosylation 2. Pathogenic ALG13 variants demonstrate strong statistical association with developmental and epileptic encephalopathy 3, with epileptic spasms representing the most common presenting symptom, often accompanied by developmental delay, intellectual disability, microcephaly, and hypotonia 4. ALG13 ranks among the top genetic causes of infantile epileptic spasms syndrome in cohort studies 5. Long-term outcomes in surviving patients (predominantly females, as males rarely survive to adulthood) include persistent seizures, severe communication difficulties, gastrointestinal and skeletal involvement, with ketogenic diet showing promising therapeutic efficacy 2. Current management focuses on symptomatic treatment including ACTH/prednisolone and vigabatrin trials 4.