Mechanistically, chromatin immunoprecipitation (ChIP) and electrophoretic mobility shift assay (EMSA) revealed SFN’s inhibition of endothelial lipase expression by preventing binding of NF-κB to endothelial lipase promoter gene (LIPG) (Lipase G, Endothelial Type), hence preserved HDL, which is beneficial in reducing atherosclerosis [151]. The gene discussed is NFKB1; the disease is atherosclerosis.