In support of Prx2 expression as a stimulator of cancer progression, when a tumor knockdown of Prx2 was performed in a mouse model it was found to inhibit CRC cell growth, and when Prx2 silencing was performed in both a polyposis mouse model and human CRC cell lines, mouse polyposis was decreased by a reduction in beta-catenin as an end-point, and beta-catenin levels are reduced in the cells in which Prx2 is silenced [49]. This evidence concerns the gene CTNNB1 and colorectal carcinoma.