Demonstrates how MEF2A activates a pathway that reduces drug sensitivity in AML, suggesting a potential treatment target.
MEF2A promoted AML progression and DOX resistance by transcriptionally upregulating ZDHHC20, thereby activating the NF-κB pathway. Targeting the MEF2A/ZDHHC20 axis represents a promising therapeutic strategy to overcome chemoresistance and improve clinical outcomes in AML patients.
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Ming et al. (2026) studied this question.
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