The underlying mechanisms by which n-3 PUFAs protected against HFD-induced liver steatosis are probably that n-3 PUFA-activated PPARα interact with proinflammatory factor NF-κB p65 with the formation of inactive PPARα/NF-κB p65 complexes [41] and the suppression of proinflammatory cytokine formation and secretion [7]. This evidence concerns the gene NFKB1 and fatty liver disease.