One report of functional studies in the NOD mouse model of T1D suggests that expression of the inhibitory receptor KIR3DL1 predisposes NOD mice to diabetes by downregulating function of regulatory T cells.9KIR3DL1 is found on telomeric KIR A haplotypes; thus, our finding that tA01 haplotypes are predisposing for T1D is consistent with the NOD result. This evidence concerns the gene KIR3DL1 and type 1 diabetes mellitus.