PD-L1 expression is upregulated in the tumor microenvironment (TME), (possibly as an immune-evasion mechanism) [8] and may be due to: (i) increased PD-L1 expression on tumor cells by intrinsic oncogenic events (e.g., loss of phosphatase and tensin homolog) [9], (ii) tumor cell PD-L1 induction in response to T-cell secreted interferon-gamma [10] and (iii) PD-L1 expression on accumulated myeloid cells and/or dendritic cells that have suppressive effects on T-cells [11]. This evidence concerns the gene IFNG and neoplasm.