We speculate that if a negative signal cannot be conveyed from SR-A to TLR3, TNF-α production might be increased through the raftlin-mediated TLR3 signaling pathway, and that this might be involved in the acceleration of T1D development in young SR-A−/− NOD mice treated with poly(I∶C). This evidence concerns the gene TLR3 and type 1 diabetes mellitus.