Collectively, these data demonstrate that the local inflammatory (n-6 PUFA-derived) eicosanoid profile in response to TNBS-induced colitis is antagonized in both genetic mouse models via two different mechanisms, that is, by increasing n-3 PUFA content in Fat-1 mice and by inducing AA deficiency in Fads1 Null mice, as seen previously [47, 48]. The gene discussed is FADS1; the disease is colitis.