Thus, the tumor necrosis induced by L19mTNFα/melphalan and the earlier infiltration of granulocytes contributing to tumor cell killing could be the key element to provide sufficient amount of tumor antigens for fuelling professional APC, which could then stimulate specific anti-tumor CD4+ TH cells and CD8+ effector CTL, leading to the complete rejection of the tumor and to the establishment of a critical reservoir of memory effector cells responsible for the accelerated rejection of the tumor upon challenge. The gene discussed is CD4; the disease is neoplasm.