CSF alleviated the atherosclerosis and hepatic steatosis in HFD-induced LDLR−/− mice by suppressing the lipid deposition and inflammation via inactivating MAPK/NF-κB signaling pathway, which reduced the levels of IL-1β, IL-6, TNF-α, iNOS, and VCAM-1, and down-regulated the expression of p65, JNK, ERK1/2, and p38. This evidence concerns the gene NFKB1 and fatty liver disease.