KRASG12C inhibitors induced a quiescent state in a subpopulation of tumor cells and these quiescent cancer cells synthesized new KRASG12C mutant protein, escaping drug inhibition through EGFR and AURKA-mediated RAS signaling activation.452 This study explained why KRASG12C inhibitor treatment only had partial responses in most lung cancer patients. Here, EGFR is linked to lung cancer.