It has been reported that genetic deficiency in ARID1A results in a reduction in chromatin accessibility at Th1-type chemokine loci in tumor cells, including colon cancer cells, and ARID1A interacts with EZH2 via its carboxyl terminal, thereby restraining the inhibitory effect of EZH2 on IFNγ signaling-mediated gene expression [57]. This evidence concerns the gene IFNG and colonic neoplasm.