Comparative studies have shown that the TLR4-MyD88-NF-κB pathway is highly conserved in mammals: Feng et al. [73] found in a porcine diabetes model that TLR4 activates IRAK-1/NF-κB via a MyD88-dependent pathway and also enhances the interferon response via the TRIF-IRF3 branch. This evidence concerns the gene NFKB1 and diabetes mellitus.