Additionally, mutations in oncogenes and tumor suppressor genes, such as phosphatidylinositol 3-phosphate kinase (PI3K)-AKT-mammalian target of rapamycin (mTOR), MYC, RAS, and hypoxia-inducible factor 1 (HIF-1), might contribute to cancer metabolism remodeling via altered mitochondrial metabolic pathways such as OXPHOS and fatty acid, glutamine, and one-carbon metabolisms [15]. This evidence concerns the gene HIF1A and cancer.