These studies have also demonstrated that a chronic inflammatory microenvironment accelerates Apc mutation-initiated intestinal tumor formation in the Apc/Muc2 double mutant mouse model of intestinal cancer [25], showing a synergistic role of Apc/Wnt/β-catenin and cytokine/Cox2 inflammatory signaling in colorectal carcinogenesis. The gene discussed is APC; the disease is intestinal neoplasm.