We validated this in the 3LL ΔNRAS mouse lung cancer cell line (26), which contains a KRASG12C mutation and has been rendered sensitive to KRASG12C inhibitors by deletion of oncogenic NRAS, as well as the CT26G12C colorectal cancer cell line (27) and the KPARG12C cell line (17), which have been engineered to express KRASG12C (Supplementary Fig. S9A). This evidence concerns the gene NRAS and colorectal cancer.