And while the conditions responsible for this phenomenon are varied22, so are the strategies to overcome it, including inhibition of the PDGF receptor using imatinib to decrease stromal cell contraction23, increasing the blood pressure within the tumor using the vasoconstrictor angiotensin II24, remodeling of the extracellular matrix using collagenase and hyaluronidase25, 26, normalizing the vascular structure within tumors using anti-VEGF antibodies27, 28, and increasing vasopermeation using the PEP fragment of interleukin-211. The gene discussed is VEGFA; the disease is neoplasm.