Rasd2, encoding a Ras-related GTP-binding protein, is involved in multiple biological processes. It is associated with the dopamine D2 receptor (DRD2) transmission pathway and has been implicated in various physiological and pathological conditions, including psychiatric disorders [2,3,4,5]. Genetic models, such as knockout mouse models, can be valuable in studying its function.

In ovariectomized mice, Rasd2 overexpression in the hippocampus alleviated depression-like behaviors, indicating its role in depression-related pathways [2]. In 5-day unpredictable mild stress (5-d UMS) exposed mice, overexpression of Rasd2 in the nucleus accumbens core (NAcc) alleviated 5-d UMS-induced depression-like behaviors and activated the DRD2-cAMP-PKA-DARPP-32 signaling pathway, highlighting its importance in stress-induced depression [3].

In uveal melanoma, silencing Rasd2 dampened cell growth, migration, invasion, and suppressed in vivo tumor growth and lung metastasis, suggesting its role in promoting cancer development and metastasis via enhancing glycolysis [1]. In thyroid cancer, genetic silencing of Rasd2 in IHH4 and TPC-1 cells impaired their malignant phenotypes, including decreased proliferation, invasion, and glycolytic activity [6].

In conclusion, Rasd2 plays a crucial role in multiple biological processes, especially in depression-like behaviors and cancer development. Mouse models, such as those with Rasd2 overexpression or knockdown, have been instrumental in revealing its function in these disease areas, providing potential therapeutic targets for treating depression and certain cancers.