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The results indicate that TRD does not represent a single, unified PGx-predicted 'poor pharmacological responder' phenotype but instead reflects a biologically heterogeneous collection of distinct PGx profiles, and actionable PGx phenotypes are neither enriched in TRD nor associated with greater TRD severity.
The hypothesis‐generating findings suggest triglyceride‐related genetic variation may identify individuals with differential responses to aspirin, and suggest triglyceride‐related genetic variation may identify individuals with differential responses to aspirin.
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