AKT1 and AKT2 are frequently activated in human cancer [16–18] following loss of the lipid phosphatase PTEN, activating mutations and/or copy number variation in EGFR or HER2 tyrosine kinase receptors, activating mutations in KRAS, in PIK3CA [19,20], [21] or in AKT1 itself [22]. The gene discussed is KRAS; the disease is cancer.