Nonetheless, depletion of TRIP6 can significantly enhance the association of A20 or CYLD with TRAF6 in ovarian cancer cells and promote the binding of A20 to TRAF6 in glioblastoma cells, suggesting that targeting TRIP6 may prove to be an effective strategy to restore the function of A20 and CYLD in restricting the NF-κB activity in these cancer cells. The gene discussed is TRIP6; the disease is glioblastoma.