The latest study that uses human CRC tissues and CRC xenograft mouse model also found the glycolytic metabolism and chemoresistance of CRC tissues were regulated via the upregulation of LOX-1/c-MYC/SULT2B1 axis, and the knockdown of LOX-1 downregulated SULT2B1 via c-MYC thus repressing glycolytic metabolism to inhibit the proliferation and chemoresistance of CRC (191). This evidence concerns the gene SULT2B1 and colorectal carcinoma.