To assess the role of Ku70 in regulating FLIP expression in prostate cancer cells, we first confirmed that Entinostat enhanced acetylation of Ku70 (Fig. 5a, Left) whilst also depleting FLIP expression in PC3 and DU145 cells (Fig. 5a, Right); subsequently, we demonstrated that, similar to Entinostat, Ku70 downregulation using siRNA caused depletion of nuclear but not cytoplasmic FLIP(L), although, unlike Entinostat, it had no effect on cytoplasmic FLIP(S) (Fig. 5b). This evidence concerns the gene XRCC6 and prostate carcinoma.