Targeting MTHFD2 disrupts mitochondrial redox homeostasis and restores venetoclax sensitivity in acute myeloid leukemia
Judith O. Sokei, Orsola di Martino, Mary Basse, Nishanth Gabriel, Liana Valin, Conner R. York, Nancy B.J. Arthur, Wujuan Zhang, Aaron R. Goldman, Francesca Ferraro, Stephen Matthew Sykes
This study identifies MTHFD2 as a critical mitochondrial enzyme in AML that supports redox homeostasis and therapeutic resistance, showing that its inhibition restores venetoclax sensitivity.
bioRxiv · Mar 20, 2026 · PreprintCancer Biology