The rationale behind choosing the latter ETS members was that ETS-1, the prototype of the ETS family, is overexpressed in latent as well as clinically manifest PCa (25), ETS-2 is also overexpressed in PCa (18), ETS-2 and ETS-1 play redundant roles (17), ETS-2 is associated with in vitro synthesized ETS-1 (26), ETS-2 interacts with ERG in vivo demonstrated by the two-hybrid system (26) and that ETV-4 is rearranged in PCa, similar to ERG (2–4). The gene discussed is ETS2; the disease is posterior cortical atrophy.