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Mechanistically, ALM activates retinoid X receptor- (RXR) through stable hydrogen bond formation, thereby upregulating caudal-type homeobox transcription factor 2 (CDX2) and cystic fibrosis transmembrane conductance regulator (CFTR), while concurrently suppressing -catenin/Snail-mediated epithelial-mesenchymal transition (EMT)

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This finding is consistent with clinical observations that some patients with tinnitus exhibit clinically normal audiograms 14,15