In fact, it was shown that mice with prostate epithelium-specific inactivation of p53 and miR-34, a direct target of p53, exhibited a significant expansion of the prostate stem cell pool and a tendency to develop early invasive adenocarcinomas and high-grade prostatic intraepithelial neoplasia (the single inactivation of either p53 or miR-34 determines a stimulation of prostate stem cell self-renewal and an increased expression of c-met and responsiveness to c-met-mediated stimulation of cell proliferation) [566]. The gene discussed is TP53; the disease is prostate intraepithelial neoplasia.