It is conceivable that the previously observed reduction of cytokines in the context of PCSK9-deficiency during sepsis28,29 may result from increases in the LDLR-mediated uptake of bacterial lipids by hepatocytes, thereby reducing the availability of these bacterial lipid PAMPs to stimulate PRRs on innate immune cells, including Kupffer cells, and consequently reducing cytokine-driven inflammation during sepsis. Here, LDLR is linked to Sepsis.