Finally, it is worth noting that, in addition to being a well-known mechanism of resistance to EGFR-TKIs, increasing research has also emphasized the significant role of MET amplification or abnormal activation in driving resistance to targeted therapies in other driver gene-positive NSCLC patients (including ALK-, RET-, ROS-1-fusion-positive, and KRAS G12C-mutant lung cancers) [46, 47]. This evidence concerns the gene MET and lung cancer.