LTβ was the most suitable candidate because (i) it was the most significantly differentially expressed cytokine (~45-fold) between the brain parenchyma- and dura-derived 4T1 cancer cell variants; (ii) its role in the regulation of inflammatory microenvironments in secondary lymphoid organs is well established [39]; (iii) recent data linked LTβ to inflammation-induced carcinogenesis [41] and (iv) the agonist-induced activation of LTβR on macrophages has been previously linked to a reduction in their nitric oxide (NO) and cytokine production in vitro [42]. Here, LTBR is linked to cancer.