To determine whether SAG overexpression is causally related to, or merely the consequence of prostate tumorigenesis, we crossed Sagfl/fl mice with Pb4-Cre;Ptenfl/fl mice, a well-established prostate cancer model in which Ptenfl/fl is deleted specifically in prostate epithelial cells by Pb4 driven Cre-recombinase to induce epithelial hyperplasia, adenomas and adenocarcinomas [33]. The gene discussed is SAG; the disease is prostatitis.