Amyloid self‐assembly of islet amyloid polypeptide (IAPP) is linked to pancreatic β‐cell degeneration and the pathogenesis of type 2 diabetes (T2D).1 The 37‐residue IAPP is secreted from the β‐cells together with insulin and acts in its soluble form as a neuropeptide regulator of glucose homeostasis (Scheme 1).1 However, under conditions of T2D, the intrinsically disordered but highly amyloidogenic IAPP self‐assembles into cytotoxic oligomers and amyloid fibrils, which mediate pancreatic inflammation and β‐cell degeneration.1, 2. This evidence concerns the gene IAPP and inflammation.