Furthermore, DNMT and HDAC inhibitors can restore apoptotic capacity by upregulating epigenetically silenced effectors such as Apaf-1, caspase-8, and p16, therefore enhancing the chemosensitivity of melanoma cells to doxorubicin, cisplatin, and etoposide [124,125,126]. The gene discussed is CDKN2A; the disease is melanoma.