Both in the early and late phases of sepsis, the activation of immune cells initiates a complex signal transduction pathway that culminates in the activation of nuclear transcription factor-kappa B (NF-κB) and mitogen-activated protein kinases (MAPK), with consequent release of large amounts of cytokines, chemokines and activation of the complement system (Munoz et al., 1991; Silasi-Mansat et al., 2010; Takeuchi and Akira, 2010; Wiersinga et al., 2014; Salomão et al., 2019). This evidence concerns the gene NFKB1 and Sepsis.