Studies performed in murine lymphoma and melanoma models have shown that pathophysiologically relevant doses of hCgA1–439 are sufficient to reduce the NGR‐TNF–induced penetration of doxorubicin in tumors by enhancing the endothelial barrier function.177In vitro studies, performed with human endothelial cell monolayers, showed that hCgA1–439 can inhibit the disassembly of VE‐cadherin dependent adherence junctions and permeability to drugs induced by NGR‐TNF. The gene discussed is TNF; the disease is lymphoma.