MYBL1, also known as v-myb avian myeloblastosis viral oncogene homolog-like 1, is a strong transcriptional activator involved in cell signaling [4]. It is associated with various biological processes, such as male meiosis where it collaborates with TCFL5 in a transcription network regulating gene expression during meiotic entry, progression, and post-meiotic differentiation [2].

In disease-related aspects, MYBL1 alterations are not limited to low-grade gliomas. For example, in gliomas, the MYB/MYBL1::QKI fusion can occur, which may be accompanied by other genetic aberrations like TP53 mutation, CDK6 and KRAS amplification in high-grade gliomas, contributing to malignant transformation [1]. In hepatocellular carcinoma (HCC), MYBL1 upregulates ANGPT2 expression, promoting tumor angiogenesis and conferring sorafenib resistance [3]. In endothelial cells, downregulation of MYBL1 contributes to atherosclerosis by repressing PLEKHM1-inducing autophagy [4]. Also, in adenoid cystic carcinoma, rearrangements involving MYBL1 are common, and these may have similar biological and clinicopathological consequences as MYB rearrangements [5,6,7].

In conclusion, MYBL1 is a key transcriptional activator involved in multiple biological processes and plays important roles in various diseases, especially in gliomas, HCC, atherosclerosis, and adenoid cystic carcinoma. Understanding the function of MYBL1 through genetic models could potentially provide new strategies for disease treatment and prevention.