Currently, it is believed that in most cancers Warburg effect is the result of normoxic or hypoxic interaction of HIF-1 overexpression, activation of oncogenes (c-Myc, Ras), loss of tumor suppressor function (mutant p53, mutant phosphatase and tensin homolog on chromosome ten (PTEN), microRNAs, and sirtuin), activation (e.g., PI3K/Akt/mTORC1, Ras-Raf-MEK-ERK-cMyc, and JAK/STA3) or deactivation (e.g., AMPK) of signaling pathways, TME components and interaction of HIF-1 with epigenetic mechanisms (reviewed in: [45]). Here, AKT1 is linked to neoplasm.