EGFR and neoplasm: Emerging evidence reveals that the occurrence of resistance to third-generation EGFR TKIs is associated with long-term drug administration and coinstantaneous selection of pre-existing resistance clones as well as the evolution of drug-tolerant presisters [6, 7], accordingly upfront combination therapy based on different targets and mechanisms is promising to prevent and overcome the resistance to third-generation EGFR TKIs by enhancing tumor cytotoxicity and concomitantly reducing pre-existing resistance clones [8].