Nmi, also known as N-Myc and STAT Interactor protein, is an interferon-inducible protein. It participates in various cellular activities and is involved in multiple signaling pathways, such as NF-κB, MAPK, JAK, TGFβ/Smad, and the regulation of genes like hTERT, IRF7. It is widely associated with processes like tumorigenesis, immune response, and inflammation, thus being of great biological importance. Genetic models, especially gene knockout (KO) mouse models, can significantly aid in studying its functions [1-10].

In a Nmi-knockout mouse model infected with Influenza A virus, the survival rate increased, weight loss decreased, viral replication was lower, and lung inflammation was attenuated compared to wild-type mice. This indicates that Nmi promotes Influenza A virus infection by facilitating the degradation of IRF7 through TRIM21, suppressing the production of type I interferon [3]. In breast cancer, knockdown of Nmi promoted cancer stem cell (CSC) traits, while overexpression inhibited them, with the regulation being at least partially through modulating hTERT signaling [2]. In sepsis, Nmi expression increased in neutrophils and monocytes, and it may exacerbate the inflammatory response through multiple receptors and signaling pathways [1].

In conclusion, Nmi is crucial in processes like viral infection, cancer development, and the inflammatory response in sepsis. Gene knockout mouse models have been instrumental in revealing its roles in these disease-related areas, helping us understand its biological functions and potentially providing new targets for treatment in these diseases.