ERCC1 and neoplasm: The inhibition of the heterodimerization of ERCC1 and XPF has been described as a “formidable target” (66); however, the instability of both proteins in the absence of heterodimerization (53–55) and the inability of incorrectly folded ERCC1-XPF to localize to the nucleus of damaged cells (67) makes it an attractive target to increase the susceptibility of tumor cells to DNA damaging chemotherapies.