Nowadays several studies have provided clues that nuclear factor kappa B (NF-κB) may be a principal regulator of pathways downstream of calorie excess that produce detrimental effects on glucose homeostasis and insulin sensitivity[4–6] and, insulin resistance is partially promoted by a shift of macrophage polarization from alterative M2 activation state to classic M1 activation state, during which process, activated M1 macrophages non-specific markers F4/80, CD68 and specific marker CD11c were upregulated, driven by NF-κB signaling [7]. The gene discussed is NFKB1; the disease is Insulin resistance.