Despite promising results, the mechanism of resistance to PI3K-AKT-mTOR pathway-targeted therapies is expected to vary dramatically between patients and within individual tumors due to a varying activity status of the pathway components, the extent of intratumoral heterogeneity, the mode and concentration of upstream stimuli, the genetic alterations present and the composition of the tumor microenvironment [35]. Here, MTOR is linked to neoplasm.