The mechanisms involved in LPS-modulated immunity and its link to T1D development are not fully understood, but previous work by Gulden et al. (169), and Wen et al. (68) has revealed the importance of toll like receptor-3 (TLR3) and Innate Immune Signal Transduction Adaptor (MyD88) in T1D onset in NOD mice; two components of the LPS/TLR4 signal transduction pathway (68, 161, 169). This evidence concerns the gene MYD88 and type 1 diabetes mellitus.