By comparing DSS-colitis in mice with either a blockade of VEGF-A activity or the knockout of the endothelial cell-specific IFN-γ response, a recent study demonstrated that the vascular barrier could be broken down by IFN-γ by destroying VE-cadherin, an adherence junction protein, and drive DSS-induced experimental colitis [86]. Here, IFNG is linked to colitis.