Except for activation by proteins, K-Ras also keeps an constitutive activation mode when mutations occurred in critical codons, characterized with G12A, G12C, G12D, G12S, G12V, G13C, and G13D in high frequency, and other low-frequency mutations.99 These mutations induced cancers by interfering with guanosine triphosphate hydrolysis to activate K-Ras constitutively. The gene discussed is KRAS; the disease is cancer.