Data indicate that: (1) IGF1R silencing led to a marked reduction in nuclear ERK and AKT expression in MCF7 cells; (2) IGF1R, but not INSR, silencing had a major effect on nuclear ERK activation in MCF7 cells; (3) both ERK1/2 and AKT proteins are capable of binding and stimulating IGF1R promoter activity; (4) cells with a disrupted IGF1R exhibited enhanced proliferation, consistent with the notion that INSR signaling drives a stronger growth response in breast cancer. Here, AKT1 is linked to breast cancer.