Although these in vitro changes in VEGF expression may not fully reflect the in vivo situation in a patient or animal, they point towards a gene-dosage-dependent effect of FOXO3 in tumor angiogenesis in NB: On one hand the activation of ectopic FOXO3 induces VEGF-A (24 kD) and on the other hand an apparent low level background activity due to slight leakiness of the ectopic construct in NB15/FOXO3 cells as already demonstrated in Figure 3D, elevates processed (21 kDa) VEGF-C steady state levels at normoxia and increases full length VEGF-C expression at hypoxic conditions. The gene discussed is FOXO3; the disease is neoplasm.