In the present study, we demonstrate that cells that have undergone EMT can promote tumor growth and neovascularization either indirectly, by promoting endothelial transdifferentiation of carcinoma cells in the tumor milieu, or directly, through the acquisition of an endothelial-like phenotype, with the central EMT-mediator FOXC2 playing a key role in these processes. The gene discussed is FOXC2; the disease is neoplasm.