Collectively, these observations support a possible role for ANGPTL4 in the promotion of metastasis in UM and provide a foundation for future studies to determine whether combined inhibition of both ANGPTL4 and VEGF could simultaneously target tumor-induced angiogenesis and metastasis, and thereby provide more effective therapies for patients with primary and metastatic UM. The gene discussed is ANGPTL4; the disease is neoplasm.