As regards the effects of 5-HT1A receptor modulation on NO availability, several investigations documented a greatly increased production of this labile mediator in IBD and in experimental colitis and highlighted its pro-inflammatory and detrimental role or vice-versa its homeostatic and protective action in the pathogenesis of intestinal injury (Perner and Rask-Madsen, 1999; Kolios et al., 2004). This evidence concerns the gene HTR1A and inflammatory bowel disease.