KRAS and cancer: ERBB2 mutations tended to be mutually exclusive (P < 0.05, OR < 1) with other RTK/MAPK pathway driver oncogenes across cancer types, e.g., EGFR, KRAS, ALK, MET, BRAF, and RET in NSCLC (Supplementary Fig. S8A), FGFR1 in breast cancer (Supplementary Fig. S8B), BRAF in CRC (Supplementary Fig. S8C), FGFR3 in bladder cancer (Supplementary Fig. S8D), and MYC in GEC (Supplementary Fig. S8E), consistent with a driver role for ERBB2 in these tumors.