Cebpe, also known as CCAAT enhancer-binding protein epsilon, is a crucial transcription factor involved in late myeloid lineage differentiation and cellular function [4]. It plays a vital role in granulocytic differentiation, and is essential for the normal development and function of neutrophils [2,3,5,6].

In acute myeloid leukemia (AML), Cebpe expression is an independent prognostic factor for overall survival (OS) and event-free survival (EFS). Low Cebpe expression is associated with a high relapse rate, and differential expression can stratify wild-type patients of multiple genes into different outcome groups. Allogeneic transplantation significantly increases the survival rate in patients with low Cebpe expression, while showing no obvious improvement in the high-expressed group [1]. In neutrophils, Cebpe is required for the generation of committed proliferative neutrophil precursors (preNeu) from granulocyte-macrophage progenitors (GMP). Loss-of-function variants in Cebpe can cause specific granule deficiency (SGD), leading to severe infections, profound neutropenia, and abnormal neutrophil morphology [3]. A gain-of-function mutation in Cebpe can cause noncanonical autoinflammatory inflammasomopathy through dysregulated transcription [4].

In conclusion, Cebpe is essential for granulocytic differentiation and normal neutrophil function. Its expression levels are closely related to the prognosis and treatment response of AML patients. The study of Cebpe in gene-knockout or conditional-knockout mouse models has provided important insights into the molecular mechanisms underlying neutrophil-related diseases and leukemia, facilitating a better understanding of disease pathogenesis and potentially guiding the development of new therapeutic strategies.