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. The gene discussed is ERCC4; the disease is neoplasm.