Based on data presented here, we propose a two-fold function for IRF5 that is cell type-specific and lends support to the 'release' model of breast cancer invasion where phenotypic changes in MECs (loss of IRF5 expression), in coordination with the infiltration and influence of inflammatory cells (high levels of IRF5 expression), lead to the breakdown of ducts and release and invasion of tumor epithelial cells [46]. This evidence concerns the gene IRF5 and breast cancer.