Failure to thrive is an important clinical feature of PMM2-CDG and is thought to be caused by a combination of poor nutritional status and impairment of the GH-IGF-1 cascade.4,5 Children with PMM2-CDG have been shown to have significantly decreased levels of ALS, IGFBP3, IGF-1 and IGF-2, and ternary complex formation compared with age-matched controls.5 The key role of GH-IGF system glycosylation in the impaired growth of children with CDG is demonstrated by the growth response of a child with PMI-CDG (formerly CDG Ib, OMIM 602579) who received mannose therapy to bypass the enzymatic defect. This evidence concerns the gene IGF2 and congenital disorder of glycosylation.