MET and nasopharyngeal carcinoma: In a study published in 2011, Lui et al. used two nasopharyngeal cancer (NPC) cell lines, HK1-LMP1 and CNE-2, and described that protein levels of regulator of apoptosis and glycolysis, TP53-induced Glycolysis and Apoptosis Regulator (TIGAR), were reduced after the treatment with two MET TKIs (by AM7, a MET inhibitor binding to the kinase linker region and extending to a hydrophobic binding site and by a tool compound SU11274), indicating that the effect is induced by METi itself and does not depend on the exact nature of inhibitor used [51].