Foxi1, a member of the Forkhead-box (FOX) gene family, is a transcription factor that plays crucial roles in cell differentiation and functional maintenance. It is involved in regulating multiple biological processes, such as ion-homeostasis, pH-regulation, and mucociliary development [3,4]. Genetic models, like KO/CKO mouse models, are valuable tools for studying Foxi1's functions.

In airway epithelium, knockout of Foxi1 in mouse ionocytes causes loss of Cftr expression and disrupts airway fluid and mucus physiology, mimicking phenotypes of cystic fibrosis. This shows Foxi1's importance in maintaining normal airway function [1]. In transgenic ferret models, Foxi1-KO led to reduced airway surface liquid volume and impaired mucociliary clearance, indicating its role in controlling airway surface liquid absorption, secretion, pH, and mucus viscosity [2].

In conclusion, Foxi1 is a master regulator in various biological processes, especially in ionocytes across different organs. Model-based research, particularly Foxi1 KO/CKO models, has revealed its significance in diseases like cystic fibrosis, highlighting its potential as a therapeutic target for airway-related disorders.