Despite the eventual achievement of glycemic control, the persistence of epigenetic modifications induced by the transient hyperglycemia, such as H3K9 monomethylation in the p65 promoter region, induces an increased NF-kB transcription, which in turn, maintains a weakly increased expression of the proinflammatory mediators (Fig. 1c). This evidence concerns the gene NFKB1 and Hyperglycemia.