Sequestration of TRAF2 and the cIAPs by Fn14 or TNFR2 could also be of relevance in cell death occurring during acute kidney injury or in pathogen-induced hyperinflammation in patients with X-linked inhibitor of apoptosis (XIAP)-deficiency triggered by TLR- and TNF- and TNFR2-mediated myeloid cell death (Lawlor et al., 2017; Martin-Sanchez et al., 2018). Here, XIAP is linked to acute kidney injury.