In contrast to the diminished neoplastic phenotype of the T2; ETV4AAA, we observed diffuse neoplasia with prevalent EGFP-positive cells, which maintained ETV4AAA, AR, and Nkx3.1 expression in the anterior prostate of the T2; Trp53LoxP/LoxP; ETV4AAA mice (Fig. 6, A and B), indicating that p53 loss is required in addition to high dosage level of ETV4 to drive prostate cancer progression. Here, TP53 is linked to neoplasm.