Breast cancer is the most common type of cancer affecting women worldwide with an increasing annual incidence. While therapies for treating localized breast cancer will frequently result in cure, mortality for metastatic breast cancer is still high due to few effective targeted treatments. Conventional chemotherapies are a mainstay for metastatic breast cancers, though durable responses are rare. Immunotherapies promise long-term responses through immune activation but have been underwhelming in breast cancer relative to other cancer types. In chapter one, I will review the mechanisms of existing therapeutic strategies that can recruit an immune response in breast cancers. From the mechanistic overview, I suggest biomarkers for combinations of conventional chemo- and immunotherapies. Since some conventional non-immunogenic therapies cause chromosomal instability, this chapter will begin with a review of mitosis, aneuploidy, chromosomal instability and the various mechanisms by which chemotherapy, targeted therapies, and endocrine therapy could stimulate an immune response. In doing so, I hope to provide a mechanistic basis for future investigations of treatment combinations in the clinical setting. By reviewing the major mechanisms of conventional therapies, I hope to convey the importance that understanding mechanism may help us to select the proper biomarker for therapies, in particular in combination with immunotherapies. Chapter two will focus on how paclitaxel chemotherapy can activate the cGAS/STING pathway to induce polarization of macrophages to a pro-inflammatory M1 phenotype. This chapter explores one of the most widely used chemotherapies in breast cancer and extends work completed in the Weaver lab investigating the mechanism of multipolar spindle formation by low dose paclitaxel. Specifically, this chapter will explore cGAS/STING as a proxy for how paclitaxel can exert cell extrinsic effects through activation of this pathway and stimulate an innate immune response. Through this work, we suggest that cGAS expression should be explored as a candidate biomarker for selecting patients for combination therapy with immune checkpoint inhibitors.