For example, TREM2 deficiency and anti-TREM2 monotherapy caused significant changes to the macrophage population infiltrating the tumor, with reduced infiltration of MRC1 and CX3CR1-labeled immunosuppressive macrophages and an expansion of a new subpopulation expressing immunostimulatory molecules, with greater numbers of PD-1-expressing CD8+ T cells and CD4+ T cells in the tre2-/- tumor-infiltrated group compared to the wild type [18]. Here, TREM2 is linked to neoplasm.