MYB, also known as c-MYB, is a transcription factor that plays crucial roles in cell proliferation, differentiation, and apoptosis through protein-protein interaction and transcriptional regulation of signaling pathways [2]. It is a key factor in regulatory networks controlling development, metabolism, and responses to biotic and abiotic stresses in plants and is frequently overexpressed in human leukemias, breast cancers, and other solid tumors, suggesting its role as an oncogene [2].

In plants, systematic screens for knockout mutations in MYB genes in Arabidopsis have started to unravel the functions of the 125 R2R3-MYB genes. These genes control many aspects of plant secondary metabolism, as well as the identity and fate of plant cells [1]. In tobacco, genome-wide identification and expression analysis of the R2R3-MYB gene family showed their involvement in plant development, hormone signal transduction, and responses to abiotic stresses [3].

In humans, the MYB gene family consists of three members. Aberrant activation of MYB has been linked to human malignancies, and much effort is being put into developing antileukemia drugs targeting MYB, such as interrupting the interaction between MYB and its cooperating factors [4,5]. In hematopoiesis, c-MYB is essential for survival, and its deletion leads to embryonic death. It is highly expressed in hematopoietic cells, and aberrant MYB expression is found in numerous solid cancer cells and human leukemia [6].

In conclusion, MYB is a highly conserved transcription factor with diverse functions in both plants and animals. In plants, it is involved in various physiological processes, while in humans, it is closely associated with cancer development. The study of MYB knockout models in plants and animals has significantly contributed to understanding its role in different biological processes and disease conditions, providing potential therapeutic targets for treating related diseases.