As inactivation of GSK-3β is one of the causes for cellular accumulation of endogenous transcriptionally active β-catenin [41], we monitored the phosphorylation status of GSK-3β at Ser9 by Western blotting after infection of cells with the avian FPV (A/FPV/Bratislava/79 (H7N7)) or human PR8 (A/Puerto Rico/8/34 (H1N1)) influenza virus strains (Additional file 1: Figures S1A and B). This evidence concerns the gene GSK3B and infection.