Indeed, many factors are involved in the mechanism of resistance in GBM, including: (i) an increase in the migration of cancer cells, angiogenesis, and proliferation, (ii) a reduction in the sensitivity to apoptosis resulting from the expression of antiapoptotic regulatory proteins, and (iii) an increase in both drug efflux expression and molecular proliferation pathways, such as Akt and NF-kB signaling (Garner et al., 2013). This evidence concerns the gene AKT1 and cancer.