In cancer cells, including PTEN deficient prostate cancer cells and glioma cells, ephrin-dependent EphA2 activation led to rapid dephosphorylation of Akt at T308 and S473 residues leading in some cases to mTORC1 inactivation and decreased cell growth and migration [86,87,88] (Figure 2A). The gene discussed is AKT1; the disease is prostate carcinoma.