NFKB1 and colitis: Several studies highlighted putative physiological effects of GILZ in mice which might potentially modulate immune responses against Yersinia. On the one hand, transgenic mice overexpressing GILZ show augmentation of thymocyte apoptosis [52], a bias to Th2 development [53] and inhibition of NF-κB signaling and Th1 response, leading to protection of mice in a colitis model [54].