In a mouse prostate cancer organoid model, high BAZ2A expression is critical for the initiation of prostate cancer of luminal origin mediated by Pten-loss whereas it is dispensable once Pten-loss mediated transformation is established, which suggest that BAZ2A-mediated epigenetic second events sensitize for key genetic events that drive tumor development [89]. This evidence concerns the gene BAZ2A and Familial prostate cancer.