In fact, in cancer cells, the continuous activation of tyrosine kinase receptors (such as HER2neu, BCR-ABL, and EGFR) and/or of the downstream phosphatidylinositol 3-kinase/AKT and RAS/MAP kinase signal transduction pathways determines the growth of mTOR activity and the consecutive activation of HIF-1. This evidence concerns the gene MTOR and cancer.