Accumulating evidence has documented that aberrant DNA methylation on CpG islands, m6A methylation on mRNA, or deregulated histone modification promotes acquired resistance.9–11 Su et al. conducted a study using human samples, identifying 216 CpG sites with varying DNA methylation levels to investigate their correlation with the characteristics and EGFR-TKI response status of patients with lung adenocarcinoma. This evidence concerns the gene EGFR and lung adenocarcinoma.