The mechanisms involved may be analogous with those in other studies, and probably involved the insulin and insulin-like growth factor (IGF) axis, which are well recognized as promoters of cellular proliferation and antiapoptosis.29 The IGF-1 receptor (IGF-1R) and insulin receptors are functional in all breast cancer subtypes.30–32 IGF-1R signaling can mediate antiestrogen resistance via cross talk with ER signaling. The gene discussed is INS; the disease is breast cancer.