EBV latent cycle protein-derived peptides could bind to HLA-E, but impair the recognition of NKG2A expressed by NK cells, thereby leading to the absence of inhibition (89). In EBV reactivation and EBV-chronic GvHD patients after HSCT, the frequency of NKG2A+CD56dim NK cell population was increased in peripheral blood (92). This evidence concerns the gene HLA-E and chronic graft versus host disease.