COL1A2 and osteogenesis imperfecta: Recent studies on a mouse model of mild to moderate OI (OI type IV) has yielded important information on disease mechanisms and possible therapeutic approaches.8 This model features a Col1a2 triple helical codon 610 Gly to Cys substitution (α2(I) G610C), corresponding to a mutation first identified in an Amish family.9 The α2(I) G610C mutation disturbs the collagen triple helix and results, as expected, in ER accumulation of the mutant‐containing misfolded collagen trimers.