They demonstrate that overexpression of both Dyrk1A and Rcan1 in endothelial cells results in greater inhibition of VEGF-mediated endothelial proliferation than in cells overexpressing Rcan1 alone, suggesting that Dyrk1A may be responsible for the increased tumor suppression observed in Ts65Dn/Rcan1+/+/− versus WT. This evidence concerns the gene DYRK1A and neoplasm.