Rac1, also known as RAS-related C3 botulinum toxin substrate 1, is a key member of the Rho GTPases. It is a cytoskeleton regulation protein that participates in crucial cellular processes such as cell adhesion, morphology, movement, and also in pathways like regulation of oxidative stress, inflammatory and immune surveillance [2,4]. Rac1 is highly expressed in various tumors and is associated with tumorigenesis, progression, epithelial-mesenchymal transition, and metastasis [1,2,3,4,5,6].

Rac1 is frequently dysregulated and overexpressed in bladder pathologies, contributing to bacterial infections, diabetes-induced bladder dysfunctions, and bladder cancers [1]. Inhibitors like NSC23766 and EHT 1864 have shown activities against bladder cancer [1]. In metastatic cutaneous melanoma, RAC1 activation is related to cancer migration, invasion, angiogenesis, and metastasis, making it a potential target for therapy [6]. Also, Rac1 has been implicated in colorectal carcinogenesis, where its signaling pathway dysregulation occurs at different steps of neoplastic progression [5].

In conclusion, Rac1 is essential in multiple cellular functions and is closely associated with various diseases, especially cancers. The study of Rac1 through gene-knockout or conditional-knockout mouse models (if applicable in the references) could potentially provide deeper insights into its functions and its role in disease development, offering new strategies for disease treatment, such as in bladder and skin cancers [1,6].