In the absence of NF-κB signaling, proteasomal degradation of C/EBPβ is increased by a JNK-independent mechanism and promotes death from TNF-α (Wang Y. et al., 2010), which suggests that we can use C/EBPβ as a target protein for the treatment of IL-17 outbreaks on co-infection. This evidence concerns the gene NFKB1 and coinfection.