Although we found that the p300 inhibitor A-485 did obviously reduce the formation of protein Kla but not significantly influenced the protein acetylation levels and other PTMs levels after ischemic stroke, exploring more specific protein Kla writer(s) in future studies will be more conducive to study the roles and mechanisms of protein Kla in regulating pathophysiological processes of relative diseases. The gene discussed is KL; the disease is ischemic stroke.