However, when T cells from NOD mice were costimulated with CD137L, they proliferated less and produced a reduced level of IL-2 than T cells from mice carrying the B10 allele of Cd137. This strongly suggested that the NOD SNPs lead to a hypo-functional mCD137 protein, which could play a role in T1D pathogenesis. This evidence concerns the gene TNFSF9 and type 1 diabetes mellitus.