Cebpb, also known as CCAAT/enhancer binding protein (C/EBP), beta, is a transcription factor that plays crucial roles in various biological processes. It is involved in pathways such as adipogenesis, immune cell differentiation, and stress-related responses, and is of great biological importance in processes like tumorigenesis, inflammation, and tissue aging [1-10]. Genetic models, especially gene knockout (KO) and conditional knockout (CKO) mouse models, are valuable tools for studying Cebpb.

In macrophage Atg5 cKO mice, autophagy deficiency leads to CEBPB accumulation. This accumulation alleviates atopic dermatitis by impairing M2 macrophage polarization, as CEBPB drives the transcription of SOCS1/3 and SQSTM1/p62-mediated autophagy normally degrades CEBPB [1]. In glioblastoma, the CEBPB + glioblastoma subcluster specifically drives the formation of M2 tumor-associated macrophages, promoting malignancy growth through molecules like MCP1 and the SPP1-Integrin αvβ1-Akt signaling pathway [2]. In a chronic stress mouse model, stress-induced epinephrine promotes the development and stemness of colorectal cancer (CRC) through the CEBPB/TRIM2/P53 axis, where CEBPB acts as the upstream transcription factor of TRIM2 which promotes p53 ubiquitination [3].

In conclusion, Cebpb is a key transcription factor involved in multiple biological functions. Studies using KO/CKO mouse models have revealed its roles in diseases such as atopic dermatitis, glioblastoma, and CRC, highlighting its potential as a therapeutic target in these disease areas.