The mechanism of IL-6 hyporesponsiveness can be IL-6R down-regulation as observed in monocytes of healthy subjects after interaction with bacterial antigens.32 Alternatively, IL-6 hyporesponsiveness may be due to attenuated gp130 phosphorylation as described in murine sepsis.33 If the latter is true in human AP, the hyporesponsiveness may be a broader phenomenon involving responses to other cytokine signaling via gp130 (eg, IL-11 and IL-27).34 This evidence concerns the gene IL11 and Sepsis.