Pancreatic β-cells undergo high levels of cellular stress in the early stages of type 1 diabetes mellitus (T1DM), including endoplasmic reticulum (ER) stress. ER stress results in the activation of the unfolded protein response (UPR), which restores homeostasis and adapts the cell to promote survival. However, in cases of prolonged or severe stress, the UPR initiates a pro-apoptotic response that results in cell death. Now, a study in Cell Metabolism examines the role of ATF6, a key mediator of the UPR, in β-cells during early T1DM development.