Table 1. Demonstrated mechanisms of acquired resistance to EGFR TKIs. The most common is the acquired mutation of EGFR Thr790Met, which has been reported in 50–60% of studied biopsies.

Secondary mutation of EGFR (T790M)

MET receptor tyrosine kinase amplification

HER2 amplification

PIK3CA mutations

Histopathological transformation from NSCLC to SCLC

Epithelial to mesenchymal transition

EGFR, epidermal growth factor receptor; TKI, tyrosine kinase inhibitor; T790M, Thr790Met; NSCLC, non-small cell lung carcinoma; SCLC, small-cell lung carcinoma.