To more directly address the question of whether elevated circulating IGF-1 levels contribute to prostate cancer, Wang and colleagues crossed transgenic mice overexpressing hepatic IGF-1 (HIT mice) with mice overexpressing human c-Myc in the prostate driven by the androgen-responsive probasin (ARR2Pb) promoter (Hi-Myc). The gene discussed is IGF1; the disease is prostate carcinoma.