Our findings that the novel anti-cancer effects of ANT2 knockdown in breast cancer cells involves TRAIL sensitization through the regulation of TRAIL receptors via JNK activation and subsequent increase of p53 activity and DNMT1 expression suggest that ANT2 suppression by shRNA might be useful as a new strategy for overcoming TRAIL-resistance in cancer therapy. The gene discussed is DNMT1; the disease is breast carcinoma.