The mechanisms responsible for the development of acquired resistance to EGFR-TKIs can be divided into three main groups: 1) secondary mutations on EGFR or EGFR amplifications, 2) activation of new signaling pathways or different gene amplification (e.g. MET), and 3) phenotypic plasticity and epithelial-mesenchymal transition or transformation to small-cell lung cancer (Delahaye et al., 2022[19]). The gene discussed is MET; the disease is small cell lung carcinoma.