Kcnn4, encoding the calcium-activated potassium channel KCa3.1, is involved in multiple biological processes. It functions in calcium-mediated signaling pathways, which are crucial for various physiological activities such as cell proliferation, migration, and immune responses [2,3,4]. Dysregulation of Kcnn4 has been associated with numerous diseases, highlighting its biological importance. Genetic models, like KO/CKO mouse models, can be valuable for studying its functions.

In mice, myeloid-specific deletion of PIEZO1/2 (upstream regulators of Kcnn4) protected from gouty arthritis, indicating that Kcnn4-mediated PIEZO-NLRP3 inflammasome activation is involved in gouty arthritis development [1]. In pancreatic cancer, knockdown of Kcnn4 attenuated cell growth, motility, and promoted apoptosis, suggesting its oncogenic role [3]. In hepatocellular carcinoma, knockdown of Kcnn4 reduced migration, invasion, and proliferation abilities of HCC cells through the MAPK/ERK pathway [4].

In conclusion, Kcnn4 is essential in calcium-activated potassium channel-mediated signaling, playing a role in processes such as inflammation, cancer cell proliferation, migration, and invasion. Mouse models with gene knockout or knockdown of genes related to Kcnn4 regulation have provided insights into its role in diseases like gouty arthritis and multiple cancers, offering potential therapeutic targets for these diseases.