PD-L1 is expressed on hematopoietic cells and can be upregulated on activation.9 Tumor cells that express PD-L1 using this pathway as a mechanism to evade recognition/destruction by the immune system.10–13 PD-L2 expression is restricted only to macrophages and dendritic cells and is also up-regulated by activation.9 Suppression of effector T-cell function by PD-1 engagement induces deletion and apoptosis,14,15 inhibition of proliferation and production of cytokine such as interleukin (IL)-2 and IFN-γ, and together with chronic antigen exposure, results in T-cell exhaustion.1 This evidence concerns the gene IFNG and neoplasm.