Importantly, this transmissible colitis risk was enhanced in germ-free wt hosts recolonized with dysbiotic fecal microbiota from Nod2-deficient mice, and conversely colonizing germ-free Nod2-deficient mice with wt microbiota reduced colitis severity, suggesting a reversible primary role of dysbiotic microbiota in intestinal tumorigenesis driven by inflammation (55). Here, NOD2 is linked to colitis.