Lo et al. reported that appropriate autophagy may protect against lung dysfunction in septic mice, while excessive autophagosomes may lead to acute lung injury through a supposed maladaptive role in the late stage of sepsis, who also indicated that the over-expression of LC3 attenuated lung injury via increasing autophagosome-lysosome fusion by raising autophagosome clearance. This evidence concerns the gene MAP1LC3A and Sepsis.