Although the deficiency of cPLA2 did not show significant effects on IBD development, the loss of FFD’s efficacy in DSS-induced cPLA2 mice indicated the importance of cPLA2 as a target of FFD-mediated stimulation of the TNF/TNFR- NF-κB anti-inflammatory pathway in the course of IBD. This evidence concerns the gene TNFRSF1A and inflammatory bowel disease.