Tumor recruitment of adaptive immune cells can have positive and negative effects to the host. The main effectors, T cells and B cells, are attracted via chemokines, cytokines, and growth factors, which continue to modulate their activity within the tumor microenvironment. Chemokines, adhesion molecules, checkpoint molecules contribute to specific lysis or immune evasion contextually. Recruited immune cells or tumor cells can secrete VEGF-A to further modulate immune cell recruitment. Cancer-associated fibroblasts can modulate the extracellular matrix to further augment effector cell migration within the microenvironment. Tumors become hypoxic, limiting effector capability. All of these factors may contribute to tumor invasion and metastasis. EMT, Epithelial-mesenchymal transition; PMN-MDSC, neutrophil-derived myeloid-derived suppressor cell. M-MDSC, monocyte/macrophage-derived myeloid-derived suppressor cell.