Together, these data suggest that Myt3 may act as a mediator of inflammatory and glucotoxic signalling pathway crosstalk, with inflammatory signalling-induced Myt3 suppression, as may occur in T1D and T2D, sensitizing β-cells to undergo cell death in response to hyperglycaemic episodes via allowing precocious Bim activation. Here, BCL2L11 is linked to type 2 diabetes mellitus.