AKR1B10 expression is lost or markedly reduced in ulcerative colitis and associated colorectal cancer (104); siRNA-mediated silencing of AKR1B10 inhibits epithelial cell proliferation (105) and targeted disruption of AKR1B8 locus leads to abnormal self-renewal of the intestinal epithelium and high susceptibility to dextran sulfate sodium (DSS)-induced colitis and associated tumorigenesis (104). Here, AKR1B10 is linked to ulcerative colitis.