It has been shown for example that the interplay between hypoxia-inducible factor-1 (HIF-1) overexpression, HIF-1 cooperation with epigenetic mechanisms, oncogene activation (cMyc, Ras), loss of function of tumor suppressors (mutant p53, mutant PTEN, miRNAs and sirtuins with suppressor functions), activated (PI3K-Akt-mTORC1, Ras-Raf-MEK-ERK-cMyc, Jak-Stat3) or deactivated (LKB1-AMPK) signaling pathways, and components of the tumor microenvironment (such as cancer-associated-fibroblasts) are likely to influence the metabolic phenotype of a tumor cell [11]. Here, AKT1 is linked to neoplasm.