The phosphorylation of RelA at Ser536, which was induced by TNF-α, caused NF-κB activation and the expression of several proinflammatory cytokines that are relevant to diabetes development, including TNF-α, which were found to be higher in the renal cortex in db/db diabetic mice and correlated with the duration of diabetes [32]. Here, NFKB1 is linked to diabetes mellitus.