demonstrated that S100A8/A9 released from CD11b+Gr1+ neutrophils activate cardiac fibroblasts, thereby promoting angiotensin II‐induced cardiac inflammation and injury.[38] In our experiments, we also found that exogenous administration of the S100A8/A9 heterodimer similarly enhances endothelial cell functions, including proliferation, angiogenesis, and cell adhesion, with S100A9 likely playing a key role in these processes (Figure S6A,B, Supporting Information). This evidence concerns the gene S100A8 and inflammation.