This included up‐regulation of Chop and increased apoptosis, along with altered mouse calvarial osteoblast differentiation in vitro.8 While determining the precise consequences of the misfolded collagen helix on ER stress and degradation pathways will be important to understand the molecular pathology of OI mutations, the key finding was that activation of autophagy by rapamycin reduced mutant collagen accumulation in the ER and improved the ability of the OI cell in vitro to deposit a collagen matrix.8 This suggested that autophagy activation may offer a useful therapeutic strategy in vivo. The gene discussed is DDIT3; the disease is osteogenesis imperfecta.