BAZ2A, also known as bromodomain adjacent to zinc finger domain protein 2A, is an epigenetic regulator. It affects the transcription of ribosomal RNA and is involved in chromatin remodeling, playing a role in maintaining genome architecture and regulating gene expression. It has been associated with various biological processes and diseases, such as cancer and tissue regeneration [2,4,5,6].

In prostate cancer, BAZ2A is required for cells with a cancer stem-like state. It binds to H3K14ac-enriched chromatin regions via its bromodomain, associates with inactive enhancers, and represses genes frequently silenced in aggressive and poorly differentiated cancer. Inhibiting the BAZ2A-BRD/H3K14ac interaction impairs prostate cancer stem cells. Also, in prostate cancer, BAZ2A represses genes through its RNA-binding TAM domain in a mechanism different from rDNA silencing, by associating with TOP2A and KDM1A [1,3].

In ground-state pluripotent stem cells, BAZ2A safeguards genome architecture by limiting the invasion of active domains into repressive compartments and regulating H3K27me3 genome occupancy in a TOP2A-dependent manner [4].

In mammalian liver regeneration, in vivo CRISPR screening identified Baz2a as a regulator, and its inhibition by specific bromodomain inhibitors led to accelerated liver healing after injuries [6].

In conclusion, BAZ2A is crucial for maintaining genome architecture, regulating gene expression, and is involved in cancer development, especially in prostate cancer, and in tissue regeneration processes like liver regeneration. The study of BAZ2A through gene knockout or other loss-of-function models has provided insights into its role in these biological processes and disease conditions, potentially offering new therapeutic strategies for related diseases.