AKT1 and cancer: Since radiotherapy is generally applied in a course of multiple fractions, cancer cells that survived after initial cycles acquire resistance through multiple cellular mechanisms including activation of NF-κB, phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt), mammalian target of rapamycin (mTOR), and become less responsive to the later cycles of radiotherapy and/or chemotherapy (Baskar et al., 2014).