Elf4, also known as myeloid elf-1-like factor (MEF), is a member of the ETS transcription factor family. It plays crucial roles in multiple biological processes, including immune response, osteogenesis, adipogenesis, and stem cell quiescence [4]. It is involved in regulating differentiation in osteogenic, adipocyte, and neuronal types, and has a significant impact on the development of the immune system [1].

In the context of diseases, gene knockout (KO) and conditional knockout (CKO) mouse models have provided valuable insights. In Elf4-/-mice, NK cell development, terminal maturation, and function are impaired, establishing ELF4 as necessary for normal NK cell function [2]. Intestinal ELF4 deficiency in mice leads to dysfunction of the intestinal barrier, gut microbiota dysbiosis, and exacerbation of alcoholic liver disease, indicating its role in maintaining gut homeostasis [3]. In IBD-related studies, bioinformatics and in-vivo tests showed that ELF4 overexpression reduced mouse intestinal inflammation by activating IL1RN transcription, suppressing inflammatory TH17 cell activity, and inducing macrophage M2 polarization [5].

In conclusion, Elf4 is essential for normal immune cell development, gut homeostasis, and regulation of inflammation. KO and CKO mouse models have been instrumental in revealing its role in diseases such as NK cell deficiency, alcoholic liver disease, and inflammatory bowel disease, providing a basis for understanding disease mechanisms and potential therapeutic targets.