Tumor-derived VEGF acts an endocrine-like hormone to induce hepatomegaly and splenomegaly owing to vessel dilation, tortuosity and activation of hematopoiesis in VEGF tumor-bearing mice, and VEGFR2, not VEGFR1, is the crucial receptor that mediates extramedullary hematopoiesis and tortuosity of vasculatures in these organs [16, 32]. The gene discussed is FLT1; the disease is neoplasm.