It is postulated that PD-L1− tumor cells escape immune surveillance through alternative mechanisms such as decreased MHC expression, increased PD-L2 expression on PD-L1− tumor cells, stromal remodeling, and epithelial–mesenchymal transition (73), as well as compensatory PD-L1 expression on host cells, including T cells (79–81), antigen-presenting cells, monocytic myeloid-derived suppressor cells (MDSCs), and host tissues (81, 82). The gene discussed is HLA-C; the disease is neoplasm.