It is well known that GLUT4 expression decreases in muscle and adipose tissues in insulin-resistant conditions such as DM [55]; in this process, some potent repressor mechanisms of the SLC2A4 gene expression have been raised, such as the inflammatory cytokine TNF, via the NFKB pathway, and the AGEs, via endoplasmic reticulum stress/inflammation [58]. The gene discussed is NFKB1; the disease is diabetes mellitus.