To simulate human prostate cancer development, we used a previously established mouse model that was crossbred between male mice with probasin promoter-driven Cre recombinase and female mice with floxed phosphatase and tensin homolog (Pten), thus Pten was conditionally knocked out in the mouse prostate, leading to prostate adenocarcinoma formation [17, 18, 37]. The gene discussed is PTEN; the disease is prostate carcinoma.