Inflammation and cell death contribute to the development of type 2 diabetes (T2D). Necroptosis, a recently characterized necrosis integrated with the extrinsic apoptosis pathway, is widely viewed as a highly proinflammatory mode of cell death. The pseudokinase MLKL is a key protein in necroptosis. However, the involvement of necroptotic markers in insulin resistance and T2D remains unclear. Xu, Du, and colleagues show that the loss of MLKL in mice prevents obesity-induced insulin resistance and glucose intolerance. These findings reveal a role of MLKL in insulin sensitivity and suggest the potential involvement of necroptotic regulators in the physiopathology of T2D.