Upon dysregulation, intensively expressed IL-6 (mostly transactivated by the nuclear factor-kappa β (NF-κβ) signaling pathway) leads to low-grade chronic inflammation, which contributes to T2DM or metabolic syndrome (MetS), as IL-6 has been demonstrated to impair insulin signaling in Ads and hepatocytes [1,5]. This evidence concerns the gene NFKB1 and metabolic syndrome.