The age of onset of type 1A diabetes is now immunologically predictable (1). Either because of a lack of sufficient understanding of the pathogenesis of type 1A (immune-mediated) diabetes or a lack of effective therapeutics directed at relevant pathogenic pathways (or both), we cannot yet prevent this disease (2). The article by Liu et al. (3) in this issue of Diabetes addresses both issues in a rat model of autoimmune diabetes (Lew.1WR1). In this genetically susceptible model, multiple viral infections or a viral RNA chemical mimic (poly-IC) activate the innate immune system leading to insulitis and β-cell destruction (4). The viruses do not appear to target islets; rather, they act by inducing inflammation such that anti-inflammatory therapy (e.g., prednisone) at the time of infection prevents diabetes (5). This model was discovered when the Kilham rat virus spontaneously infected a colony of “normal” rats with major histocompatibility complex (MHC) and dominant diabetes susceptibility loci on chromosome 4 ( Iddm 14 ) (6). The iddm14 locus encompasses the family of T-cell receptor Vβ segment genes, and in particular, a specific Vβ13 haplotype is associated with diabetes susceptibility (7). Specific T cells can be targeted by monoclonals to their Vβ sequences to prevent disease. Liu et al. analyzed the percentage and sequences of T cells with Vβ13 in islets of the rat model described above and tested whether a monoclonal antibody to Vβ13 could prevent diabetes. T cells …