The low-grade intestinal inflammation in individuals with T1D was shown to enhance the polarization of the pancreatic macrophages into the M1 classically activated macrophages [107], in which the bacterial LPS acts as an activation signal affecting the classically activated M1 macrophages by interacting with its Toll-like receptor 4 (TLR4) receptor and inducing the phosphorylation of both STAT1α and STAT1β [108]. This evidence concerns the gene TLR4 and type 1 diabetes mellitus.