Furthermore, increased post-translational modifications and delayed type I collagen secretion have been demonstrated in recessive forms of Osteogenesis Imperfecta, where the enzymes involved in collagen folding and post-translational modifications are defective (i.e. cartilage associated protein, prolyl 3-hydroxylase, serpin H1 and FKBP65) [26,36]. This evidence concerns the gene P3H3 and osteogenesis imperfecta.