At low-to-moderately high steady state levels (e.g., 10-400 nmol/L), tumor NO can activate signaling pathways by modifying/activating effector proteins such as soluble guanylyl cyclase (sGC), hypoxia-inducible factor-1α, extracellular signal-regulated kinases-1/2, protein kinase-B (Akt) via phosphoinositide-3-kinase (PI3K), and epidermal growth factor receptor (EGFR)[18]. The gene discussed is AKT1; the disease is neoplasm.