Notably, Ku70 mutations that mimic acetylation of specific lysine residues suppress the ability of Ku70 to bind DNA and render prostate cancer cell more susceptible to the effect of etoposide suggesting a role of Ku70 acetylation in the effect of histone deacetylase (HDAC) inhibitors (Chen et al., 2007[10]). This evidence concerns the gene XRCC6 and prostate carcinoma.