This effect wasexacerbated by muscle-specific knockout of Sirt3, highlighting the crucial roleof mitochondrial protein acetylation by KAT8 in heart failure progression.Overexpression of mitochondrial KAT8 increased acetylation of ATP5B at K201 inHEK293T cells, as shown by mitochondrial protein isolations followed by tandemmass tag (TMT)-based liquid chromatography and tandem mass spectrometry(LC-MS/MS) analysis. The gene discussed is SIRT3; the disease is heart failure.