Hence, in view of the clear functional and regulatory differences between TPα and TPβ, coupled with the discovery of their ability to regulate the PRK-signalling cascade implicated in PCa etiology, and in a TP isoform-specific manner, the aim of this study was to histologically evaluate expression of the individual TPα and TPβ isoforms in clinical prostatectomy specimens representative of the benign prostate and of different pathological (Gleason) grades of PCa. The gene discussed is PLAT; the disease is posterior cortical atrophy.