In addition to mitofusin-2 (MFN2), the mediator of inner mitochondrial membrane fusion, mitochondrial dynamin-like GTPase OPA1 (OPA1), remained intact in drug-exposed sarcoma cells (Figs 4A and B and S5), demonstrating that chemotherapy did not activate the mitochondrial stress sensors OMA1 zinc metallopeptidase (OMA1) and ATP-dependent zinc metalloprotease YME1L1 (YME1L1), which cleave OPA1 into its short forms (S-OPA1) under mitochondrial stress. Here, YME1L1 is linked to sarcoma.