To this end, we used an ad hoc experimental setting based on: (i) a melanoma cell line (MSR3‐mel) with an epigenetic silencing of HLA‐I expression to minimise presentation by classical molecules; (ii) an HLA‐G construct (G1m), mutated to prevent binding of its leader peptide to HLA‐E; (iii) an HCMV BACmid (AB8) lacking part of the immune evasion genes that target HLA‐I expression (i.e., US2, US3, US6). Here, HLA-E is linked to melanoma.