XIAP is regulated acutely by post-translational modifications that can determine sensitivity to cellular stresses: phosphorylation at S87 by Akt proteins reduces XIAP auto-ubiquitylation and stabilises the protein in cisplatin-treated cells (Dan et al., 2004), whereas phosphorylation at S430 by TANK-binding kinase 1 (TBK1) or the IκB kinase IKKε results in the auto-ubiquitylation and subsequent proteasomal degradation of XIAP after viral infection of cells (Nakhaei et al., 2012). This evidence concerns the gene TBK1 and viral infectious disease.