Second, sepsis-induced lymphopenia not only dampens host apoptosis of activated macrophages but also contributes to the reactivation of latent viruses [6], initiating a signaling cascade through TLR9 that leads to inflammasome activation and production of IL-18 and IL-1β [6, 56], as well as extracellular ferritin [60], with repeated TLR9 stimulation leading to the clinical appearance of a cytokine storm [19]. This evidence concerns the gene TLR9 and lymphopenia.