The constitutive interactions between TRAFs and TBK1/IKKε were confirmed at the endogenous protein level, as TRAF2, TRAF3 or TRAF6 was found to interact vigorously with TBK1/IKKε in non-stimulated 293T, HeLa and THP1 cells (Fig 2D), indicating that the TRAFs-TBK1/IKKε were pre-associated as a complex and recruited to MAVS upon infection. The gene discussed is TBK1; the disease is infection.