For example, by blocking ligand-receptor interactions, anti-CCR7 therapies may displace tumor cells out of protective niches, forcing them to accumulate in blood where they may become more accessible to other cytotoxic drugs such antibodies against established targets (e.g. CD20, CD30, CCR4, etc), or chemotherapeutics (e.g. fludarabine), or small molecule inhibitors (e.g. BCL2 inhibitors). Here, TNFRSF8 is linked to neoplasm.