CEBPB and Hyperglycemia: Both transcription factors are required for glucose‐stimulated insulin secretion and normal exocrine differentiation,[54, 55] and genetic variations in both genes have been associated with maturity‐onset diabetes of the young.[56] In addition, CEBPB was significantly activated, which has been shown to contribute to β‐cell failure in mice by causing a disequilibrium between ER protein load and its folding capacity,[57] thereby providing a molecular link between hyperglycemia, ER stress, and the UPR.