Proinflammatory IL-1β not only induces apoptosis in pancreatic beta cells,47 but also contributes to insulin residence via c-Jun N-terminal kinase (JNK).48 The causative protein of T2D pancreatic amyloid deposits, islet amyloid polypeptide (IAPP), triggers the Nlrp3 inflammasome and generates mature IL-1β49 further pointing to IL-1β as an important inflammatory mediator of T2D. This evidence concerns the gene IL1B and type 2 diabetes mellitus.