Worldwide, breast cancer is the most common cancer in females, with an annual incidence rate of 80-113 cases per 100,000 women. 1 The incidence has increased through recent decades, but the mortality rate has steadily dropped over the last 30 years. 2 Rising incidence is attributed to a combination of better diagnostic methods, lifestyle changes, hormonal replacement therapies, improved screening initiatives, and earlier detection. 3 The declining mortality rate is also associated with screening, together with modernized treatment options, including surgery, chemotherapy, targeted therapy, and radiotherapy. Today, 85% of patients with a breast cancer diagnosis can be cured with multimodal therapy. 4 However, while the aim of treatment is to cure, quality of life and prevention of acute and late treatment-associated toxicity is paramount to the decision process. 5 The St. Gallen Consensus defines four clinically relevant subtypes of breast cancer: luminal A, luminal B, human epidermal growth factor receptor 2 (HER2)-enriched, and triple-negative disease (TNBC) subtypes (Table 1). This basic classification is predominantly based on immunochemistry (IHC) markers, including estrogen receptor (ER), progesterone receptor (PR), ERBB2/HER2, and Ki-67. These clinically established, yet simple targets generally correlate with the intrinsic subtypes and still help to guide treatment decisions today. However, through whole-genome sequencing, single-cell analysis, and proteomics, new targets are on the horizon to improve treatment decision making and outcomes. 6 In the era of precision medicine, it is generally accepted that breast cancer is characterized beyond ER/PR/HER2; each subtype requires specific treatment regimens, thus necessitating the evolution of the breast cancer treatment landscape. Recent data from the Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) Study demonstrated