Among damaging missense mDNVs, the missense mDNV in SLC35A2 was of particular interest because several mDNVs in SLC35A2 are causal for malformation of cortical development with oligodendroglial hyperplasia in epilepsy (MOGHE), an epileptic syndrome with neuropathological abnormality in the brain [58], while gDNVs in SLC35A2 are causal for a developmental disorder, congenital disorders of glycosylation (CDG) [59] (Fig. 3A). The gene discussed is SLC35A2; the disease is congenital disorder of glycosylation.