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Anthocyanin is part of secondary metabolites, which is induced by environmental stimuli and developmental signals, such as high light and sucrose. Anthocyanin accumulation is activated by the MYB-bHLH-WD40 (MBW) protein complex in plants. But the evidence of how plants maintain anthocyanin in response to signals is lacking. Here we perform molecular and genetic evidence to display that HAT1 plays a new breaker of anthocyanin accumulation via post-translational regulations of MBW protein complex. Loss of function of HAT1 in the Arabidopsis seedlings exhibits increased anthocyanin accumulation, whereas overexpression of HAT1 significantly repressed anthocyanin accumulation. We found that HAT1 interacted with MYB75 and thereby interfered with MBW protein complex. Overexpression of HAT1 suppresses abundant anthocyanin phenotype of pap1-D plant. HAT1 is characterized as a transcriptional repressor possessing an N-terminal EAR motif, which determines to interact with TOPLESS corepressor. Repression activity of HAT1 in regulation of gene expression and anthocyanin accumulation can be abolished by deletion or mutation of the EAR motif 1. Chromatin immunoprecipitation assays revealed that MYB75 formed a transcriptional repressor complex with HAT1-TPL by histone H3 deacetylation in target genes. We proposed that HAT1 restrained anthocyanin accumulation by inhibiting the activities of MBW protein complex through blocking the formation of MBW protein complex and recruiting the TPL corepressor to epigenetically modulate the anthocyanin late biosynthetic genes (LBGs).