An elevated non-mitochondrial respiration in ATG3-depleted AML cells (Figure S5) is in line with ATG5 and ATG7 deficient urinary bladder cancer cells [57] and suggests that oxygen is partially used by non-mitochondrial sources like peroxisomes and NADPH-oxidases [60,61], which could result in increased cytosolic ROS [58], which we also observed by dihydrorhodamine 123 staining upon loss of ATG3 (data not shown). Here, ATG5 is linked to urinary bladder cancer.