Reply to Comments on Mal Adaptive Emergency Granulopoiesis in Decompensated Cirrhosis

In response to the points raised by Luo et al., first, we agree that focusing on the IL-6-JAK2-STAT3 pathway may overlook some other drivers of maladaptive emergency granulopoiesis (EG) and that damage-associated molecular patterns (DAMPs), such as S100A8/A9 produced and secreted by myeloid-derived suppressor cells (MDSCs), may perpetuate maladaptive EG. Thus, activation of the JAK2-STAT3 axis, which is seen in our patients with poor outcomes and is a major driver of EG,1 may have been elicited by another granulopoietic cytokine, such as G-CSF, which is elevated in these patients, or by cytokines that were not measured in our study (e.g.