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The survival of T-ALL cells after DOX treatment was correlated with the expression of Mitofusin-2 (MFN-2)A GTPase protein that mediates mitochondrial fusionWith an increase in the expression of CTE complexes as well as a proportional increase in oxygen consumption rate (OCR), and increased sensitivity to DOX was evident upon inactivating MFN-2 by CRISPR ( The anti-apoptotic protein Bcl-2 homologous antagonist/killer (BCL-2), overexpressed in some subtypes of B-cell lymphomas, regulates mitochondrial function and mediates therapeutic resistance by inhibiting the oligomerization of the pro-apoptotic Bcl-2 homologous antagonist/killer (Bak) and Bcl-2-associated X protein (Bax) proteins and by facilitating the import of GSH and complex IV subunits to mitochondria (Mattes et al., 2019)

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