Currently approved therapies primarily target key immune checkpoints, including CTLA-4, a co-inhibitory protein on T lymphocytes that interacts with B7.1 (CD80) and B7.2 (CD86) on antigen-presenting cells; PD-1, another co-inhibitory protein on T lymphocytes that engages with PD-L1 within the tumor microenvironment; PD-L1 itself; and more recently, LAG-3, which interacts with major histocompatibility complex (MHC) proteins [3]. Here, HLA-C is linked to neoplasm.