In addition to serving as a physical barrier to lymphocyte infiltration, our cell–cell interaction analysis unveiled the recruitment function of CAFs to myeloid cells, particularly neutrophils and macrophages, which are both associated with a poor clinical prognosis due to their immunosuppressive properties and roles in mediating therapeutic resistance.[60, 61, 62] Similar to the mechanism by which neutrophils attract tumor cells,[60, 63] our findings indicate that CAFs recruit neutrophils through chemotaxis, exemplified by the CXCL12‐CXCR4 Interaction. The gene discussed is CXCL12; the disease is neoplasm.