Since the PAMPs shared by pathogens, of which LPS is a prototype, do not take part in the second vicious circle of gut-origin sepsis pursuant to the “gut-lymph” hypothesis, there is abundant room for more work to validate the roles of Lcn2 in the inflammatory response triggered by DAMPs (e.g., high-mobility group box 1 (HMGB1), IL-1 family), which stimulate PRRs, in a fashion similar to PAMPs [72–74]. This evidence concerns the gene LCN2 and Sepsis.