We chose CrtapKO mice, a well‐characterized mouse model of recessive OI caused by loss of the prolyl 3‐hydroxylation complex and defective type I collagen posttranslational modifications,28 and oim/oim mice (osteogenesis imperfecta murine), which carry a spontaneous mutation in the Col1a2 gene, generate α1(I) homotrimers and are commonly used as a model of severe OI.22 This evidence concerns the gene COL1A2 and osteogenesis imperfecta.