Several mechanisms of resistance to osimertinib have been described, including the EGFR C797S that abolishes the binding of osimertinib to EGFR, as well as G796S/R in addition to a hinge pocket L792F/H mutation.24 Furthermore, c-MET amplification,19,25 ERBB2, wild-type EGFR somatic copy-number alterations, L798I,19 and SCLC transformation26 have been documented in patients resistant to third-generation EGFR-TKIs. This evidence concerns the gene EGFR and small cell lung carcinoma.