ARID2, encoding a subunit of the polybromo-associated BAF (PBAF) complex which is part of the ATP-dependent SWI/SNF chromatin remodelers, is crucial for chromatin remodeling. It is involved in diverse biological processes, such as gene expression regulation, which is essential for normal development and cellular functions [1,4,5].

In various disease-related studies, Arid2-knockout mouse models have provided insights. In normal hematopoiesis, loss of Arid2 in a conditional Arid2 knockout mouse model affects hematopoietic stem cell (HSC) differentiation in a cell-autonomous manner, resulting in decreased ability to reconstitute the lymphoid lineage, and enrichment of myeloid-biased multipotent progenitor cell signatures [4]. In liver-specific Arid2 knockout mice, hepatic steatosis occurs, and this is associated with the activation of the JAK2-STAT5-PPARγ signaling pathway due to reduced ubiquitination of JAK2, revealing its role in non-alcoholic fatty liver disease (NAFLD) [2]. In lung adenocarcinoma, ARID2 knockout in KrasG12D-based genetically engineered murine models promotes lung cancer malignant progression and shortens overall survival, suggesting its role as a tumor suppressor [3]. In melanoma, ARID2 knockout sensitizes melanoma to immune checkpoint inhibitors, with anti-PD-L1 treatment restricting tumor growth in mice bearing ARID2-knockout melanoma cells [6].

In conclusion, ARID2 is essential for normal biological processes, especially in maintaining the balance of cell differentiation and tissue homeostasis. The use of Arid2 knockout mouse models has significantly contributed to understanding its role in diseases like NAFLD, lung adenocarcinoma, and melanoma, highlighting its potential as a therapeutic target in these disease areas.