In particular, we show that elevated expression of HSAT2,3 RNAs in EwS and PCa as well as in EWS:FLI1-expressing HeLa cells and in ERG-high prostate cells was associated with activation of proinflammatory signaling, DNA damage, G2/M checkpoint, and mitotic spindle/kinetochore maintenance gene expression programs, many of which are known to be dysregulated in both cancers and, in some cases, are directly driven by EWS:FLI1 or ERG (14–16, 46). The gene discussed is FLI1; the disease is posterior cortical atrophy.