As we have noted, mutations in three broad classes of genes—proto-oncogenes (e.g., RAS), tumor-suppressor genes (e.g., APC), and genome maintenance genes—play key roles in cancer induction (Table 24-1). These genes encode many kinds of proteins that help control cell growth and proliferation (Figure 24-15). Virtually all human tumors have inactivating mutations in genes whose products normally act in various cell cycle checkpoint pathways to stop a cell’s progress through the cell cycle if a previous step has occurred incorrectly or if DNA has been damaged. For example, most cancers have inactivating mutations in the genes coding for one or more proteins that normally restrict progression through the G₁ stage of the cell cycle or activating mutations in genes coding for proteins that drive the cells through the cell cycle. Likewise, a constitutively active RAS or other activated signal-transducing proteins are found in several kinds of human tumors that have different origins. Thus malignancy and the intricate processes for controlling the cell cycle discussed in Chapter 19 are two faces of the same coin. In the series of events leading to the growth of a tumor, oncogenes combine with tumor-suppressor mutations to give rise to the full spectrum of tumor-cell properties described in the previous sections. In this section, we consider the general types of mutations that cause cancer and explain why some inherited mutations increase the risk for particular cancers. We end the section with a description of how the molecular analysis of tumors is changing the manner in which cancer is treated. Personalized medicine—the ability to diagnose individual tumors at the molecular level and to design treatments for a patient’s specific cancer—is likely to become a reality in the twenty-first century.