This observation is particularly important as it contrasts with findings in other cancers, such as in cervical cancer where CD74+ macrophages induce M2 macrophage polarization to promote immunosuppression, or in triple‐negative breast cancer where CD74 on DCs promotes an immunosuppressive microenvironment by inducing the expansion of tolerant dendritic cells and regulatory B cells.[43, 44] This discrepancy likely stems from the highly context‐dependent nature of CD74's function, which is influenced by both cell type and the tumor microenvironment. The gene discussed is CD74; the disease is neoplasm.