These data reveal that CMS1 tumors with BRAF (V600E) and CMS4 tumors with KRAS/NRAS mutations were preferentially associated with both higher 18-gene MEK activation (potential MEKi sensitivity) and higher 5-gene dasatinib sensitivity scores (see Fig. 8c “CMS1” and “CMS4” panels, “right and upper” quadrants (RUQs)), suggesting these tumors may be likely responders to a combination therapy of MEKi + SRCi in CRC. Here, KRAS is linked to colorectal carcinoma.