It is tempting to speculate that CRTAP, although it lacks enzyme activity, is the more important partner in maintaining the 3-hydroxylation complex, as patients without CRTAP lack P3H1 protein, but individuals with null P3H1 mutations, still have a residual amount of CRTAP [9] and non-lethal type VIII OI is much more frequent than non-lethal type VII. This evidence concerns the gene CRTAP and osteogenesis imperfecta.