Given the structural and functional similarities between FLI1 and ERG (5, 6) and the reported ability of ERG and other ETS factors to activate transcription in PCa cells via binding to GGAA repeats in a complex with the WT EWS protein (12), we next investigated if transcriptional activation of HSAT2,3 pericentromeric heterochromatin may also occur in ERG-driven cancers, particularly PCa, where ERG is overexpressed in more than 50% of cases (5, 8). The gene discussed is ERG; the disease is posterior cortical atrophy.