Recently, genomic profiling of advanced NSCLC with EGFR mutations at baseline has identified multiple genetic, phenotypic, and functional mechanisms that may contribute to intrinsic resistance (IR).12 Whole-exome sequencing on untreated EGFR-mutant NSCLC tumors13 and the detection of co-occurring genetic alternations, such as MET, PIK3KA, CDK4, CDK6, and NF1, in the cfDNA of advanced-stage patients before treatment with EGFR-TKI14 suggest many DNA-based biomarkers for IR prediction. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.