MYBL2, also known as B-MYB, is a transcription factor of the MYB transcription factor family. It is essential for regulating vital cellular processes such as cell proliferation, differentiation, DNA repair, and cell cycle progression [1,3]. It also plays a role in cell survival and is involved in the regulation of many biological pathways, the deregulation of which can contribute to cancer development [3]. Genetic models, like KO/CKO mouse models, are valuable for studying MYBL2's functions.

In cancer research, loss-of-function experiments have shown significant impacts. In bladder cancer, MYBL2 deficiency suppressed cell proliferation and migration both in vitro and in vivo, revealing it as an oncogene that accelerates cancer progression through transactivation of CDCA3 [2]. In prostate cancer, genetic inhibition of Mybl2 in murine models representing phenotypic plasticity decreased in vivo growth, cell fitness, and repressed gene signatures related to pluripotency and stemness [4]. In ovarian cancer, targeting the MYBL2-ATAD2 axis by Nuclease technology-mediated ATAD2 ablation inhibited in vivo tumor growth in a xenograft mouse model, highlighting this axis's role in cell proliferation [5].

In conclusion, MYBL2 is a central regulator of cell proliferation, survival, and differentiation. Through model-based research, especially KO/CKO mouse models, its crucial role in cancer development and progression in various cancer types, including bladder, prostate, and ovarian cancer, has been revealed. Understanding MYBL2's functions provides potential therapeutic targets for treating these cancers.