To investigate the mechanisms by which impaired autophagic flux causes heart failure, we disrupted autophagic initiation specifically in cardiomyocytes via either inducible (MYH6-MerCreMer driven) or constitutive (MYH6-Cre driven) knockout of ATG3, a key mediator of autophagic initiation that mediates the conversion of MAP1LC3A-I (LC3-I) to MAP1LC3A-II (LC3-II) (Nath et al, 2014; Yamada et al, 2007). The gene discussed is ATG3; the disease is heart failure.