The active effector of TH-302 is a DNA cross-linking agent previously shown to increase nuclear γ-H2AX, a key biomarker for DNA damage response pathways, in vivo following as little as 6 hours post TH-302 therapy in pancreatic tumor models [37], implying early changes in vascular permeability observed in this study may be a consequence of TH-302 cytotoxicity. The gene discussed is H2AX; the disease is pancreatic neoplasm.