AKT1 and cancer: Several mechanisms of acquired resistance to TKIs have been reported, including EGFR gene mutations [16], activation of the phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway and the Ras/MAPK pathway [17], as well as epithelial to mesenchymal transition (EMT), where acquisition of cancer stem cell-like phenotypes is associated with resistance to TKIs [10, 18–20].