The oim mutation and its biologic consequences(18–21) are strikingly similar to those found in a German child with type III OI.(6,22,23) In both instances, a frame-shift mutation in the region of the COL1A2 gene that encodes the terminal portion of the proα2(I) C-propeptide predicts the synthesis of nonfunctional proα2(I) chains. Here, COL1A2 is linked to osteogenesis imperfecta.