A subsequent treatment, such as chemotherapy plus antiangiogenic drugs, could cause the disappearance of RAS mutant clones and potentially restore sensitivity to anti-EGFR drugs.6 After anti-EGFR treatment is stopped, RAS mutant clones decay with a half-life of approximately 4 months, whereas RAS WT clones increase.7 In fact, the genetic landscape of cancer cell clones is continuously evolving for the selective pressure of different therapies.8 The gene discussed is EGFR; the disease is cancer.