During sepsis, the S100A8/A9 complex activates the classical Toll-like receptor 4 (TLR4) signaling pathway in monocytes, inducing the expression of pro-inflammatory mediators related to NF-κB, and can be released as a DAMP (Odink et al., 1987; Lagasse and Weissman, 1992). Here, S100A8 is linked to Sepsis.