Triple-negative breast cancer (TNBC) represents the most aggressive breast cancer type with poor prognosis. A significant barrier to effective treatment is the development of resistance to chemotherapy, observed in over 50% of TNBC patients, primarily driven by drug-tolerant persister (DTP) cells. These cells undergo molecular reprogramming that enhances their survival and metastatic potential, enabling them to evade chemotherapeutic agents. Central to this reprogramming are rewiring of signaling pathways, including receptor tyrosine kinases (RTKs), which are frequently dysregulated in many cancers. We found RTKs such as epidermal growth factor receptor (EGFR) to be dramatically hyperactivated in TNBC DTPs alongside upregulation and hyperactivation of non-receptor cytosolic tyrosine kinases. Thus, we aim to systematically investigate the kinase networks in DTPs, identify the candidate receptor and non-receptor tyrosine kinases, and understand how the crosstalk between them leads to TNBC drug resistance and metastasis. As kinases are actionable targets, therapeutically targeting the candidate kinases could be a promising approach to eliminate DTPs and enhance the efficacy of chemotherapy.