Influenza A viruses (IAV) cause the majority of influenza‐associated disease burden and are further classified into subtypes based on the combination of their hemagglutinin (HA) and neuraminidase (NA) surface glycoproteins.1 IAV, especially A(H3N2) virus, evolve rapidly and undergo immune driven selection.9 This occurs through changes in viral antigenic epitopes that result in evasion of immune recognition and mainly involves mutations in the HA and NA gene segments.10, 11. This evidence concerns the gene XK and influenza.