Studies have reported that, under hypoxic conditions, PFKM Ser529 achieves glycosylation through post-translation modification of acetylglucosamine to inhibit PFKM activity and reroutes glucose flux away from the pentose phosphate pathway; this results in an increased D-ribose 5-phosphate level supportive of rapid cancer cell growth through DNA and protein synthesis [41]. This evidence concerns the gene PFKM and cancer.