IL6 and Sepsis: The p38 MAPK, a well-known mediator that drives inflammation through upregulation of several pro-inflammatory cytokines such as TNF-α and IL-6 (22), and the NOD-like receptor protein 3 (NLRP3) inflammasome, able to induce the release of IL-1β and IL-18 and promote cell death by pyroptosis (23), are two of the most well characterized signaling pathways involved in the activation of the cytokine storm that contributes to organ dysfunction during sepsis.