Overall, the discovery of KLF6/Klf6 down-regulation in two different models of MYC/Myc-driven cell transformation supports the hypothesis that c-MYC germline overexpression could act as a risk factor for prostate cancer by converging on a molecular mechanism such as the functional inactivation of the KLF6 gene or gene product. The gene discussed is MYC; the disease is prostate cancer.