SOAT1 and Sepsis: Such binding results in arrays of signaling pathways including activation of NF-κb, JAK/STAT and PI3K/AKT among others, which promote inflammatory responses (32) We thus examined whether the excessive dysregulated inflammation seen in the murine model of fatal E. japonica-induced liver injury and sepsis is linked to MyD88-mediated expression of RAGE receptor and downstream signals in HCs following binding to extracellular HMGB1.