In colitis-associated cancer models, cGAS KO mice demonstrate increased intestinal inflammation, increased tumorigenesis, and tumors with higher grades of dysplasia. Colonic tumors in cGAS-deficient mice demonstrate higher ki67 and BrdU expression compared to WT mice as well as increased activation of STAT3, suggesting possible effects on tumor proliferation. This evidence concerns the gene MKI67 and colonic neoplasm.