Accumulating evidence indicates that disturbed flow and the resultant oscillatory shear stress (OSS) promote endothelial inflammation and oxidative damage, whereas laminar shear stress (LSS) maintains endothelial homeostasis by suppressing inflammatory pathways.[24, 25] Krüppel‐like factor 4 (KLF4), a shear‐sensitive transcription factor predominantly expressed in ECs, is a key mediator of LSS‐dependent vascular protection.[26, 27] Nevertheless, the potential link between KLF4‐mediated mechanotransduction and BMP6‐dependent calcification pathways requires further investigation. This evidence concerns the gene KLF4 and inflammatory response.