Based on the above results indicating that the administration of ECD and LGZGD can suppress the development of HFD-induced fatty liver, we presume that inhibition of TNF-α, NF-κB, and IRS-1Ser307 phosphorylation expressions might be major contributor to the beneficial effects of ECD and LGZGD on decreasing hepatic lipid accumulation caused by IR. The gene discussed is NFKB1; the disease is fatty liver disease.