As ER stress has previously been implicated in the development of diabetes in other models of the disease [16,22,23,24], the aim of our current study was to investigate the hypothesis that the Sdf2l1 mutation we previously found in CDs/y prevents expression of SDF2L1, precluding thereby BIP from being effectively recruited as a chaperone and hindering the triggering of the PRK, IRE1 and ATF6 pathways. Here, SDF2L1 is linked to diabetes mellitus.