Finally, considering the central role of the Rb-E2F complex in survival and proliferation and the widespread Rb pathway mutations found in human cancers, our findings could assist in better defining the etiology of tumor metabolism, in particular the perplexing phenotype of aerobic glycolysis and the lack of efficient mitochondrial oxidation of glucose despite the ostensible need for ATP in hyperproliferative cells. This evidence concerns the gene RB1 and neoplasm.