The conversion to an immune evasive microenvironment in advanced MDS is facilitated by the overexpression of immune checkpoint molecules, including the programmed cell death of protein 1 (PD-1), its ligand PD-L1, and cytotoxic T lymphocyte-associated protein 4 (CTLA-4), leading to T cell exhaustion [138], [Figure 4]. The gene discussed is PDCD1; the disease is myelodysplastic syndrome.