In tumor samples derived from patients harboring METex14 mutations, KRAS amplification occurred following treatment with crizotinib, and further investigation demonstrated that KRAS amplification rendered cells hypersensitive to growth factors and activation by RTKs other than MET; this allowed for the sustained signaling of MAPK and PI3K pathways during METex14 inhibition [137]. Here, MET is linked to neoplasm.