AKT1 and neoplasm: Considering an accumulation of damaging side effects from a combination of therapies that inhibits several canonical signaling pathways impinging upon translation initiation, and the mTOR inhibition-induced feedback activation of upstream receptors and AKT signaling that may reduce anti-tumor effects of mTOR inhibitors [49-52], targeting cap-dependent translation that could simultaneously block upstream oncogenic signals and their downstream targets would hold potential as a future therapeutic strategy against the metastatic progression of cancer.