For instance, we have previously shown that the presence of oncogenic KRAS in colon cancer cells causes a switch in CD95-signaling output from apoptosis to invasion, which is required for metastatic spread and tumor recurrence.15, 20, 21 This raises the question of how to select patients for CD95-inhibitory therapy and whether there could be genetic or epigenetic traits that may determine the response to such therapy. The gene discussed is FAS; the disease is colonic neoplasm.