Chen et al found that M2 macrophages led to a hypersusceptibility to secondary bacterial infection.36 Our data showed that compared to the control mice, Shp2 knockout mice displayed significantly lower levels of M1‐related genes (eg, IL‐6, TNF‐α, IL‐12b and inducible NO synthase [iNOS]) (Figure 3A‐D) and elevated expression of M2‐related genes including Arg1, Ym1 and Fizz1 (Figure 3E‐G), upon dual infection. The gene discussed is RETNLB; the disease is bacterial infectious disease.