Furthermore, co-occurrence of KRAS mutations with other oncogenes such as TP53 and CDKN2A in various cancers, KEAP1 and STK11 in lung adenocarcinoma, or APC and PIK3CA in CRC, may influence therapeutic response.31,32 Overall, we found significantly higher comutation rates between KRASG12C and several other oncogenes compared with KRASnon-G12C-mutant tumors, although these differences were not observed in the NSCLC and CRC cohorts. The gene discussed is TP53; the disease is cancer.