In this study, we also performed tissue recombination assays using AR-deficient and control UGMs as described above with UGEs isolated from another prostate cancer mouse model, PtenL/L:PBCre4 mice17, and observed mild pathologic changes and impaired oncogenic growth in the samples recombined with AR-deficient UGMs (Supplementary Fig. 1b, c). This evidence concerns the gene AR and Familial prostate cancer.