Although in experimental models of colitis and IBD-derived human samples the exact source of GDNF in the gut is not unequivocal, increased GDNF expression showed anti-apoptotic epithelial effects [252, 253], and is strongly upregulated in inflamed areas of CD and UC [252, 254] lending further support to the beneficial role of EGCs in modulating epithelial barrier function. The gene discussed is GDNF; the disease is inflammatory bowel disease.