In the dual-flank tumor model, HCT/0.5- and HCT/130-mono-mIL12 selectively accumulated in HER2-expressing CT26-HER2/neu tumors over HER2-negative CT26 tumors, whereas HCT/217-mono-mIL12 could not, suggesting that tumor retention only occurs above a threshold of anti-HER2 affinity, below which unbound HCT-mono-mIL12 undergoes rapid systemic clearance through diffusion out of tumors due to the tumor’s high capillary permeability (6). The gene discussed is ERBB2; the disease is neoplasm.