This is likely underpinned by IGF1Rβ/IR hybrid receptors, which allow endocrine-sensitive cancer cells to expand their ligand-binding capacity whereby insulin and IGF-1 can signal through either heterodimer or specific homodimers.36 In TamR cells, however, where there is little IGF1Rβ, IR becomes the predominant receptor driving insulin and IGF-stimulated growth. This evidence concerns the gene IGF1 and cancer.