The CSC evolution during tumor development and treatment is associated with activation of different pro-survival pathways which cause intrinsic radioresistance of tumor cells such as epidermal growth factor receptor (EGFR), phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR), wingless-type MMTV integration site family (WNT), Notch, and Hedgehog signaling [11,14,45], and different agents targeting these molecular pathways are currently in preclinical and clinical development. The gene discussed is AKT1; the disease is neoplasm.