T‐cell dysfunction is associated to an exhausted state which is characterized by high levels of multiple ICs and impaired effector functions, including T‐cell cytotoxicity and the production of effector cytokines.[30] Here, the in vitro and in vivo data consistently implied that RNase1 led to a decrease of effector cytokines (IL‐2 and INF‐γ in vitro; GB and INF‐γ in vivo) and an increase of multiple ICs (PD‐1, LAG‐3, and TIM‐3) in CD8+ T cells, which may contribute to CD8+ T‐cell dysfunction during cancer progression (Figure 2B,G and Figure 4D–I). This evidence concerns the gene IL2 and cancer.