Cooperation of HER2 and the insulin/IGF1R pathway has been previously implicated in resistance to targeted therapies, whereby in a model of trastuzumanb resistant breast cancer, HER2 and IGF1R form heterodimers, and stimulation of IGF1R leads to HER2 phosphorylation in resistant cells, but not in sensitive cells [34]. This evidence concerns the gene ERBB2 and breast carcinoma.