SLC35A2 encodes a UDP-galactose transporter that functions as an antiporter, exchanging UDP-galactose for UMP in the Golgi apparatus and transporting other nucleotide sugars including UDP-N-acetylgalactosamine 12. The protein localizes to the Golgi apparatus of neuroepithelial cells and Golgi outposts along oligodendroglial processes 3. SLC35A2 is essential for sphingolipid glycosylation and affects N-glycosylation pathways 43. Somatic mutations in SLC35A2 cause two distinct epileptic phenotypes: early epileptic encephalopathy with epileptic spasms and moderate-to-severe intellectual disability, and drug-resistant focal epilepsy with normal/borderline cognitive function 5. These mutations are associated with mild malformation of cortical development with oligodendroglial hyperplasia in epilepsy (MOGHE), characterized by increased oligodendroglial cell density and heterotopic neurons in white matter 67. Nonsense variants cause significant protein reduction, while missense variants alter protein distribution 3. MOGHE tissues show hypomyelination patterns that improve with age, suggesting developmental timing effects 3. Surgical outcomes are generally favorable, with 63.8% of patients achieving seizure freedom 5.