VHL and intestinal neoplasm: Previously, we have reported that intestine-specific disruption of Vhl (VhlΔIE) activates HIF signaling, and when these mice are crossed to the Apcmin/+ intestinal tumor model (VhlΔIE/Apcmin/+), colorectal tumorigenesis is robustly increased compared with littermate control mice (VhlF/F/Apcmin/+) [14].