Significance Basal-like/BRCA1-associated breast cancer (BC) is a very aggressive form of BC that frequently occurs in young women, with devastating effects. Since tailored therapies are lacking for this type of tumor, scientists and clinicians are searching for weaknesses that can be therapeutically exploited. Here we describe the role of the transcription factor aryl hydrocarbon receptor (AhR) in supporting BC growth by controlling reactive oxygen species (ROS) levels and the tumor-promoting features of the microenvironment. In BC cells, AhR activation mediates the link between intracellular ROS regulation and the protumorigenic functions of the surrounding immune system. We propose that tailored inhibition of AhR-regulated pathways can lead to BC eradication by pushing it beyond its ROS tolerance limit and depriving it of tumor-supporting immune cells.