Indeed, selective pharmacological blockade, antibody neutralization, or genetic deletion of inflammatory mediators such as IL-1β and inducible nitric oxide synthase (iNOS; the enzyme in β-cells responsible for nitric oxide production) can attenuate or prevent diabetes in response to encephalomyocarditis virus infection in genetically susceptible mice (210, 211), Kilham rat virus infection in the Bio-Breeding rat (20, 212–214), spontaneous diabetes in the NOD mouse (121, 215), and in other models of diabetes (216–218). This evidence concerns the gene IL1B and diabetes mellitus.