Using CRISPR to silence or knock out individual elements in HCT116 colorectal cancer cells, we found that LTR10-derived enhancers causally drive AP1-dependent gene expression at multiple loci, including genes with established roles in tumorigenesis and therapy resistance such as ATG12, XRCC4, and VCAN (57, 59, 63–65, 88–90). The gene discussed is XRCC4; the disease is colorectal cancer.