Our observations suggest that in Rab27-deficient mice, the down-regulated and altered distribution of endothelial TJ proteins (ZO-1 and Cldn5) and disorganized F-actin coincides with, and likely contributes to, the formation of dysmorphic, hyperpermeable, and dilated tumor-associated vasculature, with altered endothelial landscapes and permissive of paracellular extravasation by anticancer T cells (fig. The gene discussed is CLDN5; the disease is neoplasm.