The acquired resistance to EGFR-TKIs may be mediated by secondary EFGR mutation (T790M for first-/second-generation TKIs, loss of T790M, and secondary C797S mutation for osimertinib), bypass pathway activation (MET/HER2 amplification, KRAS/BRAF/PIK3CA mutation, and RET/FGFR3/BRAF fusion), or small-cell lung cancer transformation [14, 15]. Here, BRAF is linked to small cell lung carcinoma.