Mutations in the CRTAP gene lead to Sillence type VII OI and mutations in the LEPRE1 gene, which encodes the P3H1 protein, lead to Sillence type VIII OI, and both gene mutations result in delayed folding of the collagen chain and consequently in excessive hydroxylation of lysine residues such as LH1 and P4H1 and subsequent excessive glycosylation modifications [11–13]. This evidence concerns the gene CRTAP and osteogenesis imperfecta.