More recently, it was shown that pan-HDAC inhibition with the clinical-stage compound ITF2357/givinostat improved cardiac relaxation in murine models of hypertension- or aging-induced DD with preserved ejection fraction, and that SAHA was efficacious in a feline model of HFpEF due to slow, progressive ascending aortic banding (107–109). This evidence concerns the gene HDAC9 and dentin dysplasia.