PCK2 upregulation leads to gluconeogenesis, which can stabilize the nutrient supply under low‐glucose conditions, favoring the synthesis of critical metabolic intermediates essential for tumor growth.[28, 35] These findings suggest that the role of PCK2 in enhancing energy efficiency and redox balance is key in resistance to multiple tyrosine kinase inhibitors.[32] This metabolic flexibility highlights the importance of PCK2 in the adaptation and survival of cancer cells under adverse conditions. This evidence concerns the gene PCK2 and neoplasm.