Recent research has shown improvements in T2DM through the inhibition of oxidative stress which involves mechanisms that are associated with the toll-like receptor 4 (TLR4), pathogen recognition, the myeloid differentiation primary response 88 (MyD88), signaling within immune cells, and the NF-κB signaling pathway, a regulator of innate immunity (23). This evidence concerns the gene MYD88 and type 2 diabetes mellitus.