TKIs act on the ATP binding pocket of EGFR, inhibit EGFR autophosphorylation and antagonize tyrosine kinase signal transduction.24 First-generation (erlotinib, gefitinib, and icotinib) and second-generation (afatinib and dacomitinib) EGFR TKIs have been approved for the treatment of advanced NSCLC patients harboring EGFR-activating mutations.25 Unfortunately, resistance is inevitably acquired in most patients, at a median of 10–14 months after treatment.26 The most common reason for acquired resistance is the T790M mutation in exon 20 of EGFR. Here, EGFR is linked to non-small cell lung carcinoma.