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. This evidence concerns the gene IGF1R and neoplasm.