MET and neoplasm: In some studies, tumour heterogeneity, expression of other members of the HER family (e.g. HER-3), mutation of a HER family member (e.g. the EGFRvIII), the co-expression of other heterologous growth factor receptors (e.g. c-MET, IGF-1R), and the presence of cancer stem cells has been suggested as possible mechanisms of resistance to therapy with the HER inhibitors and cytotoxic drugs.