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These phosphatases contribute to the dephosphorylation of the downstream effector molecule PI3K, attenuate the activation of AKT, and inhibit the PI3K-AKT-mTOR signaling axis, promoting the expression of the adipose triglyceride lipase (ATGL) and the key enzyme for FAO, carnitine palmitoyl transferase (CPT1A), which inhibits T cell glycolysis and instead promotes FAO, thus reprogramming the metabolic pathways of T cells [30]