Upon endoplasmic reticulum stress (ERS), T1DM-related cytokines, including IL-1β and IFN-γ, can induce β-cells to release exosomes containing calreticulin, heat shock protein Gp96, and oxygen-regulated protein 150 (ORP150) to further exacerbate T1DM-related autoimmune diseases [38]. This evidence concerns the gene CALR and type 1 diabetes mellitus.