Based on the above-mentioned studies [7–11], which used various mouse models of cancer and chronic infection, we propose that PD1-IL2v has multiple potential molecular mechanisms of action: (i) targeting of IL-2v to PD-1+ tumor- or virus-specific T cells; (ii) strong IL-2Rα-independent binding to IL-2R via its anti-PD-1 antibody-mediated targeting to the cell surface in cis; (iii) prolonged interaction with IL-2R via anchoring to PD-1 and slow internalization of the whole complex leading to the removal of PD-1 from the cell surface, as shown in human CD4+ T cells [8]; and (iv) PD-1 blockade. The gene discussed is CD4; the disease is neoplasm.