Accordingly, targeting KDR would offer the added value of suppressing portosystemic collateralization on several levels, such as angiogenesis and flow-induced collateral remodeling, as suggested by the striking magnitude of reduction in portosystemic collateralization and collateral blood flow, as well as the downregulation of the expression of vascular remodeling markers produced by the siRNAKDR-lipoplex therapy in portal hypertensive mice. This evidence concerns the gene KDR and portal hypertension.