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Unlike nuclear DNA, mtDNA lacks protective histones and has limited DNA repair capacity, rendering it particularly vulnerable to genotoxic stress, such as from reactive oxygen species (ROS) generated during oxidative phosphorylation (OXPHOS) (31)

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Besides that, PD-1 blockade also activates AMPK and mTOR, which in turn upregulates the expression of peroxisome proliferator-activated receptor (PPAR)-gamma coactivator 1 (PGC-1), resulting in increased mitochondrial activity together with ablation of PD-1, which suppresses tumor growth [66]

32 Suppression of MTHFD2 disturbs redox homeostasis, accelerates cell death in both colorectal cancer (CRC), 74,75 and acute myeloid leukemia (AML)

Individual responses may varyconsultation with a medical professional is recommended to determine suitability