In the diabetic patient, therefore, all these molecular pathways (hyperglycemia, increased oxidative stress, and activation of receptors for advanced products of glycosylation) promote the expression of the gene for the nuclear factor kappa-light-chain-enhancer of activated B cells (Nf-kB): this leads to increased production of inflammatory mediators (such as interleukin-1) and adhesion molecules for leukocytes that favor atherogenesis [17,56,57]. Here, NFKB1 is linked to Hyperglycemia.