ROS in the tumor microenvironment can act as a double-edged sword because, on one end, promoting programmed cell death while also supporting cancer cell proliferation and survival by causing DNA mutations and impairing the activities of several tumor suppressor genes such as protein tyrosine phosphatases (PTPs), phosphatase and tension homolog (PTEN), and MAPK phosphatases, resulting in the activation of the PKD-NF-KB, PI3K-PKB/Akt, AND MAPK-ERK signaling cascades51,52. The gene discussed is AKT1; the disease is neoplasm.