While AKR1B10 has been implicated in reducing glycolytic capacity in breast cancer cells, supporting their survival under low glucose conditions and facilitating metastatic colonization in the lung (41), our Seahorse XF Glycolysis Stress tests showed that AKR1B10 depletion did not modulate compensatory glycolysis but attenuated basal glycolytic activity in CRC/GC cell lines, suggesting cancer type–specific metabolic adaptation mechanisms (fig. This evidence concerns the gene AKR1B10 and breast carcinoma.