Rbm25, an RNA-binding protein, is involved in multiple biological processes such as apoptosis, inflammation, and alternative splicing regulation [1-10]. It has been implicated in various pathways, including the CHOP-associated endoplasmic reticulum stress pathway in cardiomyocytes [1]. Rbm25's role in regulating alternative splicing of genes is crucial, influencing the production of different protein isoforms that impact cell function [3,4].

In an inducible Tet2 knockout mouse model, knocking down Rbm25 accelerated the expansion of Tet2-knockout hematopoietic cells both in vitro and in vivo, suggesting that Rbm25 levels can drive heterogeneous preleukemic clonal expansion [5]. In macrophage-specific Rbm25-deficient mice, there was inflammaging, including spontaneous arthritis and inflammation in multiple organs, which could be relieved by pharmacological inhibition of Acly, indicating Rbm25's role in restraining inflammation via ACLY RNA splicing-dependent metabolism rewiring [2].

In conclusion, Rbm25 is a key regulator in multiple biological processes. Its role in disease areas such as ischemic heart failure, rheumatoid arthritis, colon cancer, and pre-leukemia has been revealed through gene-knockout-based studies. These findings highlight the importance of Rbm25 as a potential therapeutic target and provide insights into the underlying disease mechanisms.