The absence of a full-length PB1-F2 protein has been suggested as one possible determinant for the low pathogenicity of the 2009 Influenza A H1N1 pandemic strain. Since the PB1-F2 sequence of this strain has three stop codons and its ancestors encode a full-length protein, the stop codons must have appeared recently. This suggests that the PB1-F2 protein is not evolutionary and functionally important for the new virus. We investigate the role of this protein in the evolution of influenza A viruses, and in particular in relation to the history of the new strain. We show that its evolutionary history is comparable to other, non-translated, subsequences in the PB1 segment, suggesting that PB1-F2 does not contribute significantly to the fitness of the influenza A virus.