Since a sustained presence of IL-2 in tumors is critical for producing therapeutic effects23,44, we constructed a tumor-targeting Erb-sumIL2 fusion protein, which can prolong the IL-2 half-life by avoiding renal filtration of the low molecular weight protein and by delivering sumIL-2 to the tumor tissue to activate tumor-infiltrated T cells. The gene discussed is ESR2; the disease is neoplasm.