This regulatory relationship may also be present in liver fibrosis, as miR-29a has been demonstrated to significantly reduce liver fibrosis by inhibiting HDAC4 activity, leading to increased histone H3 lysine 9 acetylation at the miR-29a promoter and subsequent upregulation of miR-29a expression, thereby exerting an antifibrotic effect [88]. This evidence concerns the gene HDAC4 and Hepatic fibrosis.