Arhgdib, also known as Rho guanosine diphosphate dissociation inhibitor 2 (RhoGDI2), is a negative regulator of the Rho guanosine triphosphate (RhoGTP)ases RhoA, Rac1, and Cdc42 [4]. It mainly functions in regulating the actin network in various cells and is involved in multiple biological processes [4].

In bladder cancer, KDM6A promotes the transcription of Arhgdib by demethylating histone H3 lysine di/trimethylation (H3K27me2/3), which in turn inhibits Rac1 and blocks metastasis [1]. In breast cancer, Arhgdib expression is significantly higher in cancer tissues compared to benign tissues, and its depletion decreases cancer cell proliferation, migration, and invasion [5]. In kidney transplantation, pre-transplant anti-Arhgdib antibodies are associated with long-term kidney graft loss, and Arhgdib gene expression in the kidney is related to allograft outcome [2,3]. In trophoblasts, PD-L1 enhances migration and invasion by upregulating Arhgdib via transcription factor PU.1 [6]. In bladder cancer, ATG7-mediated autophagy promotes Arhgdib mRNA stability, leading to cancer cell invasion [7].

In conclusion, Arhgdib plays a crucial role in multiple biological processes and diseases, especially in cancer metastasis and kidney transplantation outcomes. The research on Arhgdib using various models helps to understand its functions in different physiological and pathological conditions, providing potential targets for disease treatment.