Breast cancer (BC) is the most prevalent cancer today globally and remains the second leading cause of cancer-related deaths among women. It is stratified into three main molecular subtypes: human epidermal growth factor receptor 2 (HER2)-positive, estrogen receptor (ER)-positive and the more aggressive triple-negative breast cancer (TNBC). The disproportionate burden of TNBC among Black women is alarming. Although significant advancements in screening, diagnosis and treatment have improved BC outcomes, metastasis and drug resistance still pose a formidable challenge. The face-off between oncogenes and tumour suppressors ultimately defines the fate of cancer cells. My team is investigating the cellular, physiological, and clinical roles of the breast tumor kinase (BRK) family of non-receptor tyrosine kinases in breast cancer, with a major focus on two paradoxical members: BRK and FRK (Fyn-related kinase), which share conserved functional and structural domains. While BRK levels are elevated in over 85% human breast tumors in general, FRK is typically lost or undetected especially in TNBC. Data from my lab have shown that catalytically active BRK promotes mammary tumorigenesis. We have also shown that in TNBC, FRK gene expression is silenced by site-specific promotor methylation. I will discuss our recent data highlighting the oncogenic role of BRK in BC progression, the potential clinical implications of BRK in drug-resistant breast cancers, as well as evidence of the anti-proliferation activity of FRK in BC. Our work collectively and ultimately aims to address how BRK and FRK can be targeted to shape the therapeutic landscape of breast cancer.