PD1 activation after the exposure to its ligand PD-L1 (overexpressed by monocytes/macrophages, dendritic cells, and capillary endothelial and bronchial epithelial cells during sepsis) induces intracellular pathways interrupting the T cell receptor transduction signals and ultimately leading to reduction in IL-2 synthesis, inhibition of activation and proliferation, decreased effector functions (cytokine secretion and cytotoxicity), and accelerated apoptosis [85]. The gene discussed is PDCD1; the disease is Sepsis.