Furthermore, our finding that blockade of Notch signaling using a protein-based inhibitor of Notch1 (Notch1 decoy) resulted in decreased expression of VEGFR-1 in an in vivo model of angiogenesis may have important implications for the efficacy of inhibition of Notch signaling in settings where VEGFR-1 expression is prominent, such as in certain tumor types and in the initiation of premetastatic niches [43-45]. The gene discussed is NOTCH1; the disease is neoplasm.