However, the dual control over K-Ras expression and activity that we describe here indicates that let-7, even without oncogenic mutation, can regulate Ras activity and that this might be a general phenomenon related to the interactions between tumor suppressor genes (e.g. let-7) and proto-oncogenes (e.g. K-Ras) or oncogenes (e.g. K-Ras G12V or G12D). The gene discussed is KRAS; the disease is neoplasm.