Ahrr, also known as Aryl-Hydrocarbon Receptor Repressor, is a key regulator in multiple biological processes. It participates in the aryl-hydrocarbon receptor (AHR) pathway, regulating the induction of enzymes involved in metabolizing carcinogens like those in tobacco smoke [2]. Ahrr also plays a role in cellular growth, differentiation, and regulating cellular toxicity through the TCDD-mediated AHR pathway [1].

Ahrr deficiency in mouse models has revealed its significance. In intestinal intraepithelial lymphocytes (IELs), Ahrr -/- mice show reduced IEL representation, increased oxidative stress, lipid peroxidation, and ferroptosis due to unleashed AHR-induced CYP1A1 expression. This loss of IELs makes the mice susceptible to Clostridium difficile infection and dextran sodium-sulfate-induced colitis [3]. In head and neck cancer, Ahrr wild-type transgenic mice develop tumors more frequently than Ahrr-null mice. Ahrr is shown to induce HIF-1β expression, enhancing VEGFD production and lymphangiogenesis [4].

In conclusion, Ahrr is essential for maintaining normal cellular functions and immune homeostasis. Studies using Ahrr-deficient mouse models have provided insights into its role in diseases such as inflammatory bowel disease, certain cancers, and conditions related to smoking-associated risks. Understanding Ahrr can potentially lead to new strategies for disease prevention and treatment in these areas.