This model has allowed the study of how therapeutic resistance develops in prostate cancer through lineage plasticity with TP53 and RB1 mutations, and overexpression of SOX2 and EZH2. Just as in human patients undergoing androgen therapy, these mutations reproduced the phenotypic changes observed in sequential periods where androgen-receptor-dependent luminal cells seem to turn into androgen-receptor-independent basal cells. The gene discussed is AR; the disease is prostate carcinoma.