However, in EGFR-dependent NSCLC, where the oncogenic driver is more typically EGFR bearing a catalytically activating mutation rather than overexpression of EGFR, resistance to EGFR-targeting kinase inhibitors is very rarely associated with mutations activating RAS; rather, resistance usually is associated with additional mutations in EGFR, overexpression of other receptor tyrosine kinases (the RTKs ERBB2 and c-MET), mutations in PI3K or BRAF, or histologic transition (4, 50). Here, MET is linked to non-small cell lung carcinoma.