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In line with these findings, the reduction in free fatty acids and cholesterol abundance due to AKT1 depletion was rescued by AKT1-WT, but not by the AKT1-3K/R, in TNBC cells (Fig

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Future large-scale, long-term, thyroid-focused clinical trials with neurological endpoints are required to establish efficacy, clarify patient subgroups most likely to benefit, and translate mechanistic plausibility into evidence-based clinical practice

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