Remarkably, chronic hyperglycemia and the concurrent increased levels of advanced glycation end products (AGEs) and their receptors (RAGE) as well as OS activate NF-kB by various pathways that subsequently trigger the expression of various pro-inflammatory cytokines, including IL-1, IL-6, and TNF-α, which are crucial for the development of inflammation in diabetes and other chronic diseases [97,98,99]. This evidence concerns the gene IL6 and diabetes mellitus.