MET and small cell lung carcinoma: Various resistance mechanisms have been proposed; the most common of which include secondary EGFR mutations (such as the T790M point mutation), activation of bypass signaling pathways (including amplification of the MET (c-Met) receptor), alterations in downstream signaling, or phenotypic changes including transformation to the small cell lung cancer (SCLC) subtype or epithelial-to-mesenchymal transition (EMT) (2, 4).