Previous studies have demonstrated that administration of BRBs inhibited tumorigenesis in: Apc1638+/− mice, inflammation‐driven CRC in Muc2−/− mice,[5] CRC patients,[6] and lead to polyp regression in familial adenomatous polyposis (FAP) patients.[7] FAP patients inherit a mutated copy of the APC gene, APC loss in an ISC activates the WNT pathway, and is the earliest known event in CRC; a key feature of inherited and sporadic (≈90%) CRCs. Here, APC is linked to colorectal carcinoma.