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doi: 10.3390/ijms23179738 133

This gene targeting led to the creation of transgenic mice, or designer mice, that replicated human disease

When blocking glucose metabolism, tumor cells rapidly adapt to metabolic inhibition by switching energy pathways (e.g., glutaminolysis or fatty acid oxidation), limiting the efficacy of glycolysis inhibitors like 2-DG or HK2-targeting agents [129]

Notably, pharmacological inhibition of either AMPK or autophagy partially restores cell viability but fails to rescue ATP levels, suggesting that hyperactivated mitophagy consumes residual functional mitochondria, thus perpetuating a deleterious feedback loop 32