While it has been proposed that active AR 3′-UTR shortening represents a further mechanism of PCa progression [38], permitting AR to evade regulation by tumour-suppressive miRs, such miR-34a and miR-34c [15], there is currently no evidence for reduced miR binding and consequently higher AR protein levels following AR 3′-UTR shortening. The gene discussed is AR; the disease is neoplasm.