We have also previously reported that COP1-mediated c-Jun degradation may play a pathogenic role during anthrax infection, which causes cell cycle arrest and inhibition of the proliferation of vascular endothelial cells, intestinal progenitor cells, T cells, and B cells [40,41,42,43], leading to vascular vessel leakage and breakdown of the intestinal barrier and adaptive immune system. Here, JUN is linked to anthrax infection.