ARID5B, a member of the AT-rich interactive domain (ARID) protein family, has been implicated in multiple biological processes. It may play a role in chromatin remodeling as part of the SWI/SNF chromatin remodelling complex [3]. It is also involved in regulating gene expression, with potential implications in normal and malignant hematopoiesis, B-cell development, and function [1,2].

In mouse models, Arid5b overexpression led to a reduction in the proportion of circulating B cells, immature and mature B-cell fractions in the peripheral blood and bone marrow, and follicular B cells in the spleen. There were also defects in B-cell activation and increased mitochondrial oxygen consumption rate in B cells [2]. In addition, deletion of Arid5b in mice resulted in a decrease in the proportion of immature B cells but an increase in large and small Pre-B cells, along with enhanced fatty acid uptake and oxidation in Pre-B cells. Decreased ARID5B expression in humans is a risk factor for B-cell leukemia [4].

Overall, ARID5B is crucial for B-cell development and function, regulating fatty acid metabolism and proliferation at the Pre-B cell stage. Mouse models, especially those with Arid5b overexpression or deletion, have provided valuable insights into its role in B-cell-related processes and the risk of B-cell leukemia [2,4].