(69) explored the mechanism of resistance to another third-generation EGFR TKI, rociletinib, in 43 NSCLC patients by detecting circulating tumor DNA (ctDNA), and found that 26% of patients developed resistance to rociletinib through MET gene amplification, which was the most common molecular mechanism of rociletinib resistance in the study. The gene discussed is EGFR; the disease is neoplasm.