Siglec‐F+ neutrophils create a profibrotic environment to activate fibroblasts by releasing TGFβ, TNFα, and IL‐1β to contribute to renal fibrosis.[8] Neutrophils with Siglec‐Fhigh signature are also found in cardiovascular inflammation, including atherosclerotic vessels and myocardial infarction‐injured heart, using single‐cell transcriptomics combined with cell surface epitope detection sequencing.[100] These findings suggest the possibility that targeting the profibrotic Siglec‐F+ neutrophil subpopulation may ameliorate fibrosis in multiple organs. The gene discussed is IL1B; the disease is renal fibrosis.