Xia et al. demonstrated that M2 TAMs promoted TNBC tumor growth via IL-1β-activated IL-1 receptor 2 (IL-1R2), whereas the IL-1R2 blockade strongly attenuated macrophage recruitment, M2 TAM polarization, and CD8+ T cell depletion, thereby reducing the tumor burden and prolonging the survival period [207]. Here, IL1R2 is linked to neoplasm.