AKT activation in cancer most commonly occurs as a result of amplifications, gain-of-function and loss-of-function mutations, or deletions of AKT pathway genes, including those encoding AKT’s upstream/downstream modulators, such as growth factor receptors (e.g., EGFR), PIK3CA, the p110α catalytic subunit of PI3K, Ras, PTEN, neurofibromin (NF1), serine/threonine kinases (LKB1), and cyclin-dependent kinase inhibitors (p21WAF1 and p27KIP1), and these have been detected in numerous epithelial and hematologic malignancies [7, 180]. This evidence concerns the gene NF1 and cancer.