AKT1 and neoplasm: Metabolic reprogramming of cancer cells is the result of an interaction between HIF-1α, activation of oncogenes (cMyc, Ras), loss of tumor suppressor function (mutant p53 and mutant phosphatase and tensin homolog PTEN), activation (PI3K/Akt/mTOR, Ras/Raf/MEK/ERK/cMyc, Jak/Stat3), and deactivation (LKB1/AMPK) of signaling pathways [159].