Compared to animals with wildtype TLR4 expression (TLR4+/+), female NOD mice carrying a homozygous TLR4 defect (TLR4−/−), showed significant acceleration of diabetes development, with a younger age at diabetes onset (TLR4+/+ 177±22 d, TLR−/−: 118±21 d; p<0.01). This evidence concerns the gene TLR4 and diabetes mellitus.