Taken together, these results indicate that while NSAIDs exhibit anti-angiogenic benefits, irrespective of TMPRSS2-ERG fusion state, the main factor defining their anti-PCa effect does not appear to involve anti-angiogenic activities but rather significant impact on proliferation, especially in the fusion-driven prostate tumorigenesis state (compared to no effect on proliferation in the Hi-Myc+/− mice prostate). The gene discussed is TMPRSS2; the disease is posterior cortical atrophy.