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This immediate-early glycolytic increase within minutes of TLR-stimulus, is controlled by the TBK1-IKKε-Akt signaling axis to activate the rate-limiting glycolytic enzyme hexokinase 2 (HK2), which is essential for supporting de novo synthesis of fatty acids for ER and Golgi expansion 6

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The clinical significance of GS lies in the potential for mild hyperbilirubinemia to be mistaken for a sign of liver disease highlighting the importance of accurate diagnosis and patient education[21]