Our results have important clinical implications for patients with recessive OI caused by mutations in CRTAP or LEPRE1. The absence of both encoded proteins in patient fibroblasts when either the CRTAP or LEPRE1 gene has a null mutation, most likely explains the overlapping skeletal phenotype seen in individuals with recessive OI that results from mutations in these genes [1], [4], [5], [6], [7], [8], [9]. Here, P3H1 is linked to osteogenesis imperfecta.