Inflammatory bowel disease (IBD) patients are at increased risk of colorectal cancer (CRC)1. Tumor initiating events in colitis-associated cancers (CACs) differ significantly from sporadic CRC2. In CACs, hyperactivity of wnt/beta-catenin signaling typically occur without adenomatous polyposis coli gene mutations commonly seen in sporadic colon cancers. This suggests distinct mechanisms cause dysregulation of wnt signaling in CACs. A20 (TNFAIP3) is a ubiquitin-editing enzyme, linked to IBD, with roles in dampening inflammation3.