Conversely, HRP tumors were infiltrated with more inactive monocytes (Figure 4C) and M2 macrophages with severely impaired antigen‐presenting functions (Figure 4D), which indicated that insufficient tumor antigen signaling in the HRP group may fail to fully activate TAMs, allowing them to polarize into immunosuppressive M2 macrophages under the influence of an aberrant TIME.[31] Therefore, we proposed anti–CSF1/CSF1R agonists as a potential therapeutic strategy for HRP tumors to inhibit macrophage infiltration and M2 differentiation.[32]. Here, CSF1R is linked to neoplasm.