Consistent with these findings, comet assays showed that AR gene silencing was sufficient to induce massive chromosomal DNA breakage in several melanoma cells, irrespective of endogenous levels of AR expression (Fig. 5 A), which was accompanied by induction of γ-H2AX, a marker of the DNA damage response (Bonner et al., 2008; Fig. 5, B and C). Here, H2AX is linked to melanoma.