BETi (I-BET151) not only mitigates the immune response against pancreatic β cells, but also enhances their proliferation and function, thereby increasing insulin secretion and inhibiting the development of type 1 diabetes.171 Although BRD2 and BRD4 have the same activity to inhibit INS transcription, only BRD2 can inhibit fatty acid oxidation in β cells.172 Intriguingly, in Drosophila melanogaster, the BET protein Fs(1)h is required in fat body cells for a normal lifespan as well as metabolic and immune homeostasis. Here, INS is linked to type 1 diabetes mellitus.