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Specific AML genetic subtypes may harbor genotype-encoded dependencies on de novo serine/glycine biosynthesis, linking oncogenic drivers such as FLT3-ITD, NUP98::KDM5A fusions, and KMT2A rearrangements to upregulation of the serine synthesis pathway, including phosphoglycerate dehydrogenase (PHGDH), phosphoserine aminotransferase 1 (PSAT1), and serine hydroxymethyltransferase 2 (SHMT2) [11,41]

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This finding provides new clues and insights for understanding the neurobiological mechanisms of TD and exploring more effective treatments

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91,212 These agents mediate by disrupting the CD44-HA attachment as well as inhibiting the expression of the CD44 and downstream effectors like NF-KB, JNK