Bach1, also known as BTB and CNC homology 1, is a transcription factor that regulates multiple physiological processes, including heme homeostasis, oxidative stress response, and cell cycle [5]. It is involved in various signaling pathways and plays a crucial role in development, metabolism, and disease [5]. Genetic models, such as knockout (KO) and conditional knockout (CKO) mouse models, have been instrumental in studying its functions.

In cancer, studies using mouse models have shown that antioxidants can stabilize Bach1, promoting KRAS-driven lung cancer metastasis through increased glycolysis [1]. Also, Bach1 controls angiogenesis gene transcription in lung cancer, and antioxidants increase tumor vascularity in a Bach1-dependent manner [2]. In atherosclerosis, EC-specific Bach1 knockout mice have reduced atherosclerotic lesions, indicating Bach1's role in atherogenesis [3]. In the liver, hepatocyte-specific Bach1 deletion in male mice on a high-fat diet improves glucose homeostasis and insulin resistance [4]. Cardiac-specific BACH1 knockout in mice protects against angiotensin II-and transverse aortic constriction-induced cardiac hypertrophy and fibrosis [6].

In conclusion, Bach1 is a key regulator in multiple biological processes. The use of KO/CKO mouse models has revealed its significant roles in diseases such as cancer, atherosclerosis, metabolic disorders, and cardiac hypertrophy. Understanding Bach1's functions provides potential therapeutic targets for these diseases.