Deletions of COG complex subunits lead to type II congenital disorders of glycosylation (CDG II) and are strongly associated with cerebral atrophy, developmental delay, hypotonia, ataxia and epilepsy (Foulquier et al., 2006; Kodera et al., 2015; Reynders et al., 2009; Paesold-Burda et al., 2009; Fung et al., 2012; Rymen et al., 2012; Lübbehusen et al., 2010; Huybrechts et al., 2012; Shaheen et al., 2013; Wu et al., 2004; Morava et al., 2007; Zeevaert et al., 2009; Foulquier et al., 2007). This evidence concerns the gene ALG2 and epilepsy.