Klf4, also known as Krüppel-like factor 4, is a key transcription factor. It contains a zinc finger domain and is predominantly expressed in terminally differentiated epithelial tissues. Klf4 is involved in various biological processes such as cell proliferation, migration, invasion, and differentiation, and participates in multiple signaling pathways. It can act as both a tumor suppressor and an oncogene, depending on the context, and also plays a crucial regulatory role in inflammation, making it an important target for research in cancer and inflammatory diseases [2,3,4].

In lung cancer research, loss of USP10 in mice downregulates Klf4 expression and accelerates KrasG12D-driven lung adenocarcinoma initiation and progression, indicating that USP10-Klf4-TIMP3 axis is a potential therapeutic target in lung cancer [1]. In atherosclerotic lesions, vascular smooth muscle cells (VSMCs) undergo a phenotypic switching in a Klf4-dependent manner. Klf4 enhances the metabolic switch to glycolysis through increasing PFKFB3 expression, and inhibiting glycolysis suppresses Klf4-induced VSMCs phenotypic switching [5].

In conclusion, Klf4 has diverse biological functions, being involved in processes like tumorigenesis, inflammation, and cell phenotypic switching. Gene-knockout mouse models, such as the loss of USP10-mediated down-regulation of Klf4 in lung cancer and Klf4-dependent VSMCs phenotypic switching in atherosclerosis, have significantly contributed to understanding Klf4's role in these disease areas, providing potential therapeutic targets for cancer and atherosclerotic diseases.