These include the emergence of poorly immunogenic tumor clones with a low neoantigen burden; the downregulation of major histocompatibility complex (MHC) molecules on tumor cells, thus curtailing neoantigen presentation [10]; or the upregulation of PD-L1 and PD-1 through the activation of IFN-γ (concomitant with Teff cell activation) [11]. Here, HLA-C is linked to neoplasm.