Bcl-xL overexpression in both INS-1E and human EndoC-βH1 β-cells protects them from both cytokine- and palmitate-induced apoptosis, proving its ability to counteract classical death signals from T1D (i.e., proinflammatory cytokines) and T2D (i.e., palmitate). Here, BCL2L1 is linked to type 2 diabetes mellitus.