Besides, we measured the ratio of LC3-I to LC3-II and the protein levels of a well characterized autophagic substrate, p62/SQSTM1, which binds to LC3 and is specifically degraded as a result of complete autophagic flux; the conversion to LC3-II increased and the level of the p62 was reduced with the increase of infection time and infection concentration, indicating that autophagy was induced and promoted upon EV71 infection. Here, SQSTM1 is linked to infection.