Although this energy rearrangement is not present in all cancers, renal cell carcinoma is thought to be driven by metabolic changes due to the high rate of mutations in genes that control metabolism, such as von Hippel-Lindau (VHL) in the hypoxia pathway, mammalian target of rapamycin (mTOR), phosphatase and tensin homolog deleted on chromosome ten (cf), and mesenchymal epithelial transition factor in the PI3K (phosphatidylinositol-3-kinase) -Akt (protein kinase B) -mTOR pathway (6). This evidence concerns the gene AKT1 and renal cell carcinoma.