Reactivation of MAPK or cyclin/cdk deregulation [13], epithelial-to-mesenchymal transition (EMT), SRC activation [12] and upregulation of other RTKs (AXL [13], FGFR [22], or c-MET [23] have all been implicated in resistance in ESCC, but there is no clear indication of which is the optimal target in the largest proportion of ESCC patients. This evidence concerns the gene MET and esophageal squamous cell carcinoma.