The expression of PD-1 by exhausted T cells indicates their lost capability to execute their effector function, while the interaction between PD-1 and PD-L1/2 leads to the inhibition of T cell activation and cytokine secretion, i.e., interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and interleukin 2 (IL-2), and helps to maintain immune homeostasis by avoiding the onset of autoimmunity [22]. The gene discussed is IL2; the disease is Autoimmunity.