To determine whether this regulation is cell autonomous rather than based on the difference in tumor malignancy between PtenPC−/− and PtenPC−/−; Arid1aPC−/− mice, we silenced ARID1A in human and mouse PCa cells and verified that ARID1A depletion sensitized PCa cells to TNF-α stimulation, as evidenced by the increases in p-IKKα/β and p-P65 levels and the nuclear accumulation of p65 and p50 (Fig. 3c and Supplementary Fig. 3b). This evidence concerns the gene ARID1A and neoplasm.