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In addition, a recent study also revealed that the liver-specific Ulk1 and Ulk2 double knockout mice, where Ulk1 and Ulk2 were key components of the unc-51-like autophagy activating kinase 1 (ULK1) complex that functions upstream of the autophagy pathway, were more resistant to APAP-induced liver injury

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Future studies should aim to clarify the pharmacokinetic and pharmacodynamic mechanisms underpinning their interaction, with an emphasis on identifying specific patient populations that may be at increased risk