Atg5 itself is an essential autophagy regulator, and functions to mediate the lipidation of Atg8, therefore increasing the elongation of the phagophore for autophagosome formation (Romanov et al. 2012; Sakoh-Nakatogawa et al. 2013). We hypothesize that in the ypt6Δ strain, the overexpression of ATG5 suppresses the autophagy defect by increasing the formation of autophagosomes.