While the inhibition of PFK-1 activity through glycosylation has been shown to promote the PPP and growth of cancer cells[66], loss of FBP1, whose activity directly opposes that of PFK-1 by converting F-1,6-P2 to F-6-P, has also been observed in human liver, colon, gastric and breast cancers[90,91]. This evidence concerns the gene FBP1 and breast cancer.