JUN and colorectal cancer: 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).