Interestingly, Fagan et al. [33] showed that tamoxifen-resistant ER+ cells showed a reduction in the number of IGF-1 receptors, whereas the number of insulin receptors and AKT phosphorylation levels remained unaltered when stimulated with Insulin and IGF-2, suggesting that both IGF-1 and IGF-2 signaling may support resistance of breast cancer cells to therapies. The gene discussed is INS; the disease is breast carcinoma.