MafK, a member of the small Maf family of basic region leucine zipper (bZIP)-type transcription factors, forms homodimers or heterodimers with cap 'n' collar (CNC) proteins and Bach proteins [3]. It lacks a transcriptional activation domain, and its homodimers act as transcriptional repressors, while its heterodimers can be involved in transcriptional activation or repression depending on the partner [3]. MafK is associated with pathways like stress response, detoxification, and is linked to various diseases such as ulcerative colitis, diabetes, neuronal disorders, thrombocytopenia, and carcinogenesis [1,4].

MafK overexpressing transgenic mice were more susceptible to Salmonella mucosal infection, with higher mortality, weight loss, intestinal damage, and inflammation. MafK promoted epithelial cell apoptosis via caspase-3 activation, contributing to Salmonella dissemination and inflammation [1]. In non-immune cells, MafK mediates chromatin remodeling to silence IRF8 expression in a cell-type-specific manner [2]. β-cell-specific Mafk overexpression in transgenic mice impaired pancreatic endocrine cell development, with disorganized islets, reduced β-cell proliferation, and altered expression of β-cell-related genes [6]. Mafg -/-:Mafk -/- double knockout mice had lens defects during embryogenesis, with mis-expression of genes related to the cytoskeleton, cell cycle, extracellular matrix, and ephrin signaling [5].

In conclusion, MafK plays crucial roles in various biological processes such as pathogen infection response, gene silencing, and organ development. Mouse models, including overexpression and knockout models, have been instrumental in revealing its functions in diseases like Salmonella-induced mucosal infections, and in understanding its role in pancreatic and lens development.