Mice with mutations in Col1a1 (Brtl and Col1a1Jrt/+model; Boskey et al., 2013; Eimar et al., 2016) or Col1a2 (OIM model; Lopez Franco, Huang, Pleshko Camacho, & Blank, 2005) have dentin mineralization defects consistent with OI‐associated dentinogenesis imperfecta (DI) in humans (Foster, Ramnitz, et al., 2014). The gene discussed is COL1A1; the disease is osteogenesis imperfecta.