Given S100A8/A9 quickly induced the release of CCL2 and CCL6 from neutrophils in the early stage of TAC (Figure 2H-J), which may be key signals for the recruitment of CCR2+ myeloid cells, particularly monocytes, into injured hearts during the late stage of HF, we first assessed the effect of neutrophil S100A9-KO on Ang II-induced CCL2 and CCL6 expression and macrophage migration in vitro. The gene discussed is CCL2; the disease is hydrops fetalis.