A study conducted by Cheon and group on IBD showed that GS inhibited IL-1beta- or lipopolysaccharide (LPS)- induced ICAM-1 expression, NF-κB transcription activity and IκB phosphorylation/degradation in human Caco-2 cells and rat non-transformed IEC-18 cells (Cheon et al., 2006). This evidence concerns the gene NFKB1 and inflammatory bowel disease.