ATG8h and ATG8i are an unique sub-group of the nine ATG8 proteins encoded in Arabidopsis genome that do not need ATG4 protease for cleavage to expose their C-terminal Gly residue for lipidation and subsequent recruitment to the autophagosomal membranes. We previously showed that clathrin light chain 2 (CLC2) participates autophagy through interacting ATG8h and ATG8i and knocking out ATG8h and ATG8i simultaneously compromised autophagy, and as a result, enhanced the resistance to a biotrophic fungal pathogen. In this study, we further investigate the roles of ATG8i in disease resistance by over-expressing ATG8i. Our results showed that over-expression of ATG8i enhanced the resistance to biotrophic bacterial and fungal pathogens but compromised the resistance to a toxin secreted from a necrotropic fungal pathogen. The enhanced resistance to the biotrophic pathogens were correlated with the elevated levels of both callos deposition and H2O2 induced by Golovinomyces cichoracearum infection.