Instead, the stabilized IL-2–anti-IL-2 complex preferentially acts on cells with a high level of IL-2Rβ-γc intermediate-affinity receptors, such as NK and CD8+ T cells, inducing their proliferation and STAT phosphorylation, decreasing TIL markers of “exhaustion”, and improving anti-tumor responses65. The gene discussed is CD8A; the disease is neoplasm.