Recently, mutations in the human TRAPγ and TRAPδ subunits (SSR3 and SSR4, respectively) were found to result in loss of TRAP and congenital disorders of glycosylation (CDG) [56,143,264,265], suggesting that TRAP plays a direct or indirect role in the biogenesis of N-glycosylated proteins (MIM 300090 and 606213). This evidence concerns the gene SSR4 and congenital disorder of glycosylation.