BATF, short for basic leucine zipper ATF-like transcription factor, is a crucial transcription factor. It is involved in multiple biological processes, including T-cell differentiation, activation, and exhaustion, as well as in the regulation of regulatory T (Treg) cells, group 2 innate lymphoid cells (ILC2s), and natural killer (NK) cells. BATF interacts with other transcription factors like IRF4, and is associated with pathways related to immune responses and tumorigenesis [1,2,3,4,5,6,7,8,9]. Genetic models, such as knockout (KO) and conditional knockout (CKO) mouse models, are valuable tools for studying BATF's function.

In CAR-T cell models, depletion of BATF improves antitumor performance by enhancing resistance to exhaustion and promoting the formation of central memory cells [1]. Overexpression of BATF in CD8+ T cells expressing a chimeric antigen receptor (CAR) promotes the survival and expansion of tumor-infiltrating CAR T cells, and counteracts T cell exhaustion [2]. In Treg cells, BATF deficiency inhibits tumor growth, and high BATF expression is associated with poor prognosis in lung cancer, kidney cancer, and melanoma [3]. In NK cells from AML patients, deletion of BATF enhances their function against AML [9].

In conclusion, BATF is a key regulator in immune-related biological processes. KO/CKO mouse models have revealed its significant role in diseases like cancer, mainly by influencing the function and fate of immune cells such as T cells, Treg cells, and NK cells. Understanding BATF's function provides potential therapeutic targets for treating cancer and other immune-related disorders.