The mechanisms involved in activation of a PI3K-Akt are constitutively activated receptor tyrosine kinases (IGF/IGFR, ErbB, FGF/FGFR systems) leading to constitutive activation of PI3K; phosphatase and tensin homolog (PTEN) gene function, PI3K mutations: aberrant activation of Akt, eIF4E, 4E-BP1, and p70S6K, where these alterations trigger a cascade of biological events, i.e., from cell growth and proliferation to survival and migration, which contribute to tumor progression. This evidence concerns the gene PTEN and neoplasm.