The following section (Section 4) will build on this framework to systematically dissect how RNS regulate tumor cell proliferation (via PI3 K/Akt and AMPK pathways), apoptosis (through mitochondrial dysfunction and NF-κB modulation), invasion/metastasis (by activating MMPs and Rho GTPases), and metabolic reprogramming (via glycolysis and glutamine catabolism remodeling) – unraveling the functional consequences of RNS’s source- and concentration-dependent properties in shaping tumor cell fate. The gene discussed is AKT1; the disease is neoplasm.