NFKB1 and diabetes mellitus: In this context, the excessive production of superoxide anion radical (•O2−) in the mitochondrial electron transfer chain (ETC) [13] activates classical metabolic events evidenced in the course of DM, such as: increased polyol pathway activity [19]; increased formation of advanced glycation end products (AGEs) [25–27]; protein kinase C (PKC) [27,28] and nuclear transcription factor κb (NFκb) [29] activation; and increased hexosamine pathway flux [28].