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). This evidence concerns the gene MYC and prostate cancer.