Moreover, chronic inflammation is now also considered a hallmark of type II diabetes and exposure of human islets to metabolic stresses increases levels of IL-1β and chemokines that may contribute to insulin secretory failure and β-cell death in type II diabetes.44 Thus, our data suggest that Tpl2 inhibition may also be a relevant therapeutic strategy to preserve β-cell function and/or mass in type II diabetes. Here, MAP3K8 is linked to type 2 diabetes mellitus.