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]. The gene discussed is IFNG; the disease is neoplasm.