Cancer is fundamentally a mitochondrial metabolic disease. Tumor cells depend on two “fermentation” fuels(glucose and the amino acid glutamine) to keep their rapid growth engine running. This reliance is the modern expression of the classic Warburg effect, where cancer cells favor glycolysis (glucose..lactate) even when oxygen is plentiful, and they also use glutaminolysis to generate substrate‑level phosphorylation inside the mitochondria. Because many parasites use the very same metabolic pathways (they too rely heavily on glucose and glutamine for energy), anti‑parasitic drugs such as benznidazole, febendazole and ivermectin can be surprisingly effective against certain cancers. These agents disrupt the enzymes and mitochondrial processes that both parasites and cancer cells need to maintain their fermentative metabolism, essentially “starving” the tumor. Tumor cells are incapable of switching to fatty acids or ketone bodies as primary fuels when glucose and glutamine are removed. Unlike normal adult cells, which can readily oxidize fats and ketones through efficient mitochondrial respiration, cancer cells remain locked into their primitive, low‑efficiency energy strategy. In other words, as a primitive, single‑celled‑like organism, they lack the metabolic flexibility to perform oxidative phosphorylation on fatty acids or ketones. This metabolic inflexibility is what makes a ketogenic, low‑glucose/low‑glutamine approach a powerful adjunct to conventional cancer therapy.