STZ versus controls: −56.5%, P < 0.05), suggesting a diabetes-induced repression in the activity of the Nf-κB. EA in diabetic animals induced an increased phosphorylation of the complex Nf-κB-p65 (STZ + EA versus STZ: +91%,  P < 0.05) and a concomitant increase in the phosphorylation of the IκB-α (STZ + EA versus STZ: +42.1%, P < 0.05), suggesting an EA-induced inactivation of the IκB-α with a parallel increase in the activity of the Nf-κB. Here, NFKB1 is linked to diabetes mellitus.