Given that KRASG12D inhibition reactivated EGFR/wild-type RAS signaling, we sought to test whether the current EGFR-specific monoclonal antibodies (cetuximab and panitumumab) [6] or kinase inhibitors (gefitinib) [42] were capable of eliminating reactivated RAS effector signaling and sensitizing KRASG12D-mutant CRC cells to KRASG12D inhibitor treatment. The gene discussed is EGFR; the disease is colorectal carcinoma.