To determine if the severe phenotype observed after myocardial infarction in Tie2-CreERT2;Wt1lox/lox+Tamoxifen animals was solely due to diminished vessel formation or to the combination of reduced vascularization with enhanced immune invasion , we examined the effects of conditional deletion of Wt1 restricted to endothelial cells only by using an additional Tamoxifen-inducible endothelial specific Cre line (VE-cadherin-CreERT2 (VE-CreERT2)). The gene discussed is TEK; the disease is myocardial infarction.