The influenza M158–66 epitope reproducibly selects a dominant public TRAV27/TRBV19+ TCRαβ in HLA-A*02:01+ donors that can cross-recognize naturally occurring M158–66 peptide variants, seemingly limiting the establishment of mutant strains within the circulating pool of human influenza A viruses and conferring universal immunity to influenza in A*02:01+ individuals [45]. This evidence concerns the gene HLA-A and influenza.