On one hand, the generation of a pro-oxidant microenvironment in early stages of tumor development, and at moderate and non-toxic levels, activates cancer cell survival signaling cascades (e.g., MAPK/ERK1/2, p38, c-Jun N-terminal kinase (JNK), PI3K/Akt) and prompt tumor angiogenesis through the release of pro-angiogenic factors (e.g., VEGF, FGF) and extracellular matrix degrading enzymes (e.g., matrix metalloproteinases- MMPs). Here, AKT1 is linked to neoplasm.