In recent years, ESCC was found to respond to immune checkpoint inhibitors, demonstrating survival benefits and therefore significantly changing the current therapeutic algorithms (see also Fig. 1).36–42 Through blockade of the programmed death receptor 1 (PD-1) on cytotoxic T-cells, its ligand (PD-L1) on tumor cells, or CTLA-4 receptor on T-cells, cancer cell-mediated immune escape could be downregulated and anti-tumor immune response could be promoted. The gene discussed is PDCD1; the disease is neoplasm.