Srsf3, also known as SRp20, is the smallest member of the serine/arginine rich (SR) protein family. It is an important multi-functional splicing factor, regulating various aspects of RNA biogenesis and processing, and is involved in many cellular processes such as cell cycle, proliferation, migration, and invasion [1,2,3,5,6]. It has been linked to multiple diseases, especially cancer, where its deregulation is a key feature [1,2,3,5,6].

In germ cells, conditional knockout of Hnrnph1, which recruits Srsf3, causes abnormal splicing events, affecting meiosis-related genes and communication between germ cells and Sertoli cells, leading to male and female sterility. This shows that Srsf3 is crucial for proper germ cell development through its role in alternative splicing [4]. In colorectal cancer, knockdown of Srsf3 reduces the secretion of VEGF, inhibiting the migration, invasion, and tube formation of endothelial cells, indicating its role in tumor angiogenesis [7]. In Kupffer cells, Srsf3 deficiency in obese mice impairs metabolic parameters, while overexpression preserves a certain cell population and improves metabolic responses, suggesting its role in obesity-related insulin resistance [8].

In conclusion, Srsf3 plays essential roles in various biological processes including germ cell development, tumor angiogenesis, and metabolic regulation. Gene knockout (KO) and conditional knockout (CKO) mouse models have significantly contributed to understanding Srsf3's functions in germ cell-related infertility, cancer angiogenesis, and obesity-related insulin resistance, highlighting its potential as a therapeutic target in these disease areas.