AKT is frequently activated in cancer through a variety of mechanisms, including amplification of growth factor receptors (e.g., HER2/neu and EGFR), amplification or mutation of phosphatidylinositol 3-kinase (PI3K), amplification or mutation of AKT isoforms, and inactivation of phosphatase and tensin homolog (PTEN) or inositol polyphosphate-4-phosphatase type II (INPP4B) or VHL [3, 4]. This evidence concerns the gene PIK3CA and cancer.