Cdc42, a member of the Rho family of small GTPases, is a master regulator of the actin cytoskeleton. It controls cell motility, polarity, and cell cycle progression, and is involved in signaling downstream of Ras [2,4]. It plays key roles in diverse cellular events like cell division, invasion, migration, and filopodia formation [1]. Its activity is crucial for normal cell division, development, and gametogenesis in female vertebrates [3,6].

Cdc42's deregulation is associated with various pathogenic processes, especially cancer. Overexpression of Cdc42 is observed in several cancers, and it is linked to poor prognosis and tumor metastasis [4,5,7]. In Ras-related cancers, enhanced Cdc42-signaling facilitates Ras-mediated cellular transformation, tumorigenesis, and metastasis [5]. Also, Cdc42 dysregulation has been implicated in cellular and tissue aging, as well as in the development and progression of aging-related pathologies such as neurodegenerative and cardiovascular disorders [8].

In conclusion, Cdc42 is essential for normal cellular functions such as cell polarity establishment and gametogenesis. Its dysregulation is strongly associated with cancer and aging-related diseases. The study of Cdc42 through various models, including potential KO/CKO mouse models, helps in understanding its role in these disease conditions, potentially leading to the development of therapeutic strategies targeting Cdc42 and its associated pathways.