Herein, and based on the similarities of yeast and cancer metabolism, we speculate that in addition to the posttranslational modifications of the mammalian Pgk1, such as phosphorylation and O-GlcNAcylation, that promote the switch from the tricarboxylic acid cycle, into lactate production, dipeptide binding may constitute an additional regulatory mechanism to promote the glycolytic capacity of cancer cells48,53. This evidence concerns the gene PGK1 and cancer.