On the other hand, pharmacological or genetic targeting of eNOS showed reduced tumor growth and progression in pancreatic and other K-Ras-driven cancers, supposedly through the regulation of H- and N-Ras on the Golgi and reducing NO levels near the plasma membrane, the subcellular domain of K-Ras, offering potential avenues for therapeutic interventions [295]. The gene discussed is NRAS; the disease is neoplasm.