Finally, two carefully designed preclinical experimental approaches for evaluating Gnetin C’s potential in chemoprevention, interception and therapy in prostate cancer involved transgenic mouse models: one depicting a high-risk premalignant prostate tissues overexpressing MTA1 on the background of Pten heterozygosity (R26MTA1; Pten+/f; Cre+) [54] and another representing MTA1-overexpressing advanced prostate cancer (R26MTA1; Ptenf/f; Cre+) [53]. This evidence concerns the gene MTA1 and prostate cancer.