Recently, periodic mutation profiling of ctDNA from stage IV GC patients by Next Generation Sequencing (NGS) revealed the complex and heterogeneous molecular mechanisms for crizotinib resistance after two months of treatment, including reoccurrence of MET amplification, multiple secondary MET mutations (D1228, Y1230, V1092, G1163 and L1195), a remarkable increase in the relative copy number of the FGFR2 gene as well as mutations in other downstream and related elements [58]. Here, MET is linked to gastric cancer.