These findings underscore that while transcription factors like HIF-1α boost AQP4 expression in hypoxia, post-transcriptional mechanisms (e.g., microRNA-mediated mRNA suppression) act in the opposite direction to restrain AQP4, suggesting a complex balance that fine-tunes AQP4 levels during stroke and that could become potential therapeutic targets if better understood. The gene discussed is AQP4; the disease is Stroke.