In addition to peptides derived from classical HLA, the immune checkpoint-related non-classical HLA-G, frequently expressed in GBM [21], provides the nonameric peptide VMAPRTLFL, which when loaded on HLA-E results in HLA-E:peptide complexes reported to have the best affinity for inhibiting CD94/NKG2A and activating CD94/NKG2C receptors [22,23]. The gene discussed is HLA-G; the disease is glioblastoma.