Following IS, increased incidence of infections occurs, mainly in the form of pneumonia and urinary tract infections.43, 44 The underlying mechanism is insufficient antigen‐presentation of monocytes/macrophages and DCs in peripheral immune organs, resulting from downregulation of MHC class II and co‐stimulatory molecules and remarkable reduction of proinflammatory cytokines.45 Herein, we speculated that the pronounced upregulation of MS4A4A in the spleen following IS might reflect a phenotypic switch of monocytes from the proinflammatory M1 phenotype to the anti‐inflammatory M2 phenotype. The gene discussed is MS4A4A; the disease is infection.