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Notably, fructose metabolism synergistically amplifies this metabolic reprogramming by bypassing EMP rate-limiting steps (e.g., phosphofructokinase (PFK)) and enhancing nicotinamide adenine dinucleotide phosphate (NADPH)-mediated redox buffering capacity, thereby exacerbating CRC aggressiveness and positioning ALDOB inhibition as a therapeutic vulnerability [6, 7]