This crucial restructuring of tumour cell metabolism is controlled by classical oncoproteins and tumour suppressors, such as c-myc, hypoxia inducible factors, p53, mammalian target of rapamycin (mTOR), phosphatidylinositol 3-kinase (PI3K) and Akt (protein kinase B)4, 5. The gene discussed is TP53; the disease is neoplasm.