Interestingly, the differentially accessible sites within these tumors were enriched for IRF motifs and associated with IFN-regulated genes.23 Considering our results, and the ability of DNA accessibility to play a role in the IFN response in vivo, it is possible that in tumor samples wherein TRAF3IP1 is more accessible, its increased expression may help inhibit the anti-tumor immune response at least partly through mitigating IFN signaling.27 This mechanism, however, would require a thorough experimental validation to hold preliminary clinical relevance. Here, TRIM63 is linked to neoplasm.