In this regard, IFN-γ release can be seen as a ‘‘double-edged sword’’, where acute IFN-γ is beneficial to the initial T-cell-mediated anti-tumor efforts (immune cell recruitment and activation) as well as in inducing MHC expression on tumor cells, whereas chronic IFN-γ exposure induces further mutations in tumor cells and leads to PD-L1 upregulation84. The gene discussed is HLA-C; the disease is neoplasm.