HDAC9 and rhabdomyolysis: The role of class I HDAC in AKI is controversial: blocking class I HDAC activity with MS-275 resulted in a more severe tubular injury in mouse models of AKI induced by folic acid or rhabdomyolysis [16], whereas HDAC inhibition with phenylthiobutanoic acids enhanced renal recovery in a mouse ischemia/reperfusion model [24].