However, the absence of a requirement for Tak1 in the CSM raises an interesting conundrum, since on the one hand, Tak1 is required downstream of TNFR to activate JNK signaling (Vidal et al. 2001; Delaney et al. 2006; Stronach et al. 2014; Andersen et al. 2015), and on the other, it plays crucial roles in the activation of Rel in the immune response to pathogenic infection (Silverman et al. 2003; Park et al. 2004). Here, TNFRSF1A is linked to infection.