MET and neoplasm: Furthermore, mutations, overexpression, or amplification of the MET gene in some tumor types resulted in aberrant HGF/c-Met axis activity, which induced cell motility and proliferation, promoted tumor development, and led to resistance to radiotherapy and targeted drug therapy in multiple cancers (Minuti et al., 2012; Barrow-Mcgee et al., 2016; Bahrami et al., 2017).