It has been recently established that agonist-activation of TPα and TPβ can, in turn, lead to PRK1-catalysed H3Thr11 phosphorylation in prostate cancer cells, representing the first demonstration that agents other than androgens can induce this key epigenetic modification and recognized gate-keeper of androgen-induced transcriptional activation [35, 47]. This evidence concerns the gene PLAT and prostate carcinoma.