Arid4b, a chromatin protein, is a member of the Sin3a corepressor complex and plays a crucial role in regulating gene expression, epigenetic regulation, and cell fate decisions. It is involved in various biological processes such as embryonic stem cell differentiation, cell cycle regulation, and apoptosis, and is associated with the PI3K/AKT pathway [1-7]. Genetic models, especially knockout models, have been instrumental in studying its functions.

In glioma cells, Arid4b knockdown suppresses cell proliferation, induces G1 phase arrest, and increases apoptosis via the PI3K/AKT pathway. It also reduces cell migration and invasion [1]. In mouse embryonic stem cells, Arid4b -deficient cells have less proliferative capacity during differentiation, and there is a slight increase in Caspase -3 activation suggesting early apoptosis. Arid4b is also involved in suppressing interferon -related genes during meso/endoderm differentiation [2,4]. In breast cancer cells, heterozygous knockout of ARID4B using Nuclease technology attenuates some aggressive phenotypes like reduced proliferation and migration [3].

In conclusion, Arid4b is essential for proper embryonic stem cell differentiation, cell cycle regulation, and apoptosis. Its study through gene knockout models has provided insights into its role in glioma, breast cancer, and during embryonic stem cell differentiation. Understanding Arid4b functions may offer new strategies for treating related diseases.