Here, we addressed this important issue using a mouse prostate tumorigenesis model, triggered by Pten loss, which recapitulates the entire process of human prostate tumorigenesis with sequential formation of lesions such as hyperplasia/LGPIN, HGPIN and eventually adenocarcinoma in a manner dependent on the length of Pten inactivation [33]. The gene discussed is PTEN; the disease is prostatitis.