Consistent with KRAS being a key oncogenic driver, alterations in KRAS were highly mutually exclusive with other driver alterations in the RTK/MAPK pathway, including EGFR, ALK, MET, ERBB2, BRAF, RET, and ROS1 in non-Sq NSCLC (Fig. 3b); BRAF, FGFR2, ERBB2, RET and NTRK1 in PDAC; NRAS, BRAF, and ERBB2 in CRC; and ERBB2 in endometrial. This evidence concerns the gene RET and colorectal carcinoma.