EGFR and neoplasm: Among the 16 responders in the osimertinib-relapsed cohort, eight had EGFR-based and/or MET-based resistance, and eight did not have resistance mechanisms identified through NGS, suggesting that at least some of the tumors with unknown resistance may reflect non-genetic mechanisms leading to TKI resistance but continued sensitivity to EGFR-directed and MET-directed inhibition by the combined action of amivantamab and lazertinib or the immune-based anti-tumor effects of amivantamab.