In marked contrast with HEV development in lymph nodes which depends on dendritic cell expressed LTαβ engagement of LTβR in EC, HEV neogenesis in mouse tumours is driven by CD8+ T- and/or NK cell secretion of LTα3 and IFN-γ which induce expression of peripheral node addressin (PNAd, a ligand for L-selectin) and the arrest chemokine CCL21 respectively. The gene discussed is CD8A; the disease is neoplasm.