Metastatic melanomas are resistant to therapy for a variety of reasons, including their ability to bypass cell-cycle checkpoints [14], express insufficient amounts of critical apoptosis proteins [15], maintain p53 wild-type status, which allows them to upregulate DNA repair genes (DDB2, XPC) [16], and express an oncogenic form of BRAF that gives them an advantage in growth [17]. This evidence concerns the gene DDB2 and melanoma.