For example, a patient subpopulation consisting of mutant TP53 and wild-type KRAS in metastatic and chemotherapy-refractory CRC showed better clinical outcomes when treated with the EGFR antibody, cetuximab8, suggesting that the efficiency of molecular targeted therapy (e.g., cetuximab, trastuzumab) depends on TP53 status, in combination with other genetic alterations, even though the mode of action of the targeted therapy is not directly relevant to p53 signals. The gene discussed is TP53; the disease is colorectal carcinoma.