We not only found increased p62 accumulation in our in vitro and in vivo experimental models in response to AL-LC, but also obser-ved an increase in p62 levels in explanted human hearts from AL cardiomyopathy patients, further supporting a decrease in autophagic clearance as the cause for impaired autophagic flux. This evidence concerns the gene SQSTM1 and laryngotracheoesophageal cleft.