Despite the fact that our proof-of-concept BsB exhibits a modest potency (due to its moderate affinities for the MHCII and CTLA-4) and a short circulating half-life (which limited its exposure), a short course of treatment reproducibly delayed the onset of T1D in NOD mice treated at an early age (between 4 to 6 weeks of age, Figure S2) and when they were older (between 9 to 12 weeks of age), albeit with modest benefits (Fig. 4). This evidence concerns the gene CTLA4 and type 1 diabetes mellitus.