When upregulated in response to glucose deficiency and oxidative stress, SIRT1 deacetylates β-catenin, causing its translocation from the nucleus to the cytoplasm, attenuates glycolysis, and positively correlates with fatty acid oxidation. This promotes the shift in glycolipid metabolism, facilitating tumor development in colorectal carcinoma. This evidence concerns the gene SIRT1 and colorectal carcinoma.