Global data on cancer statistics ranks breast cancer at the highest position in terms of incidence and cancer-associated mortality in females. Despite advancements in medical imaging procedures that aid in the early diagnosis and treatment of Stage I breast cancer patients, little success has been made in tackling the more advanced and metastatic cases. Tumors that have disseminated become challenging to eliminate due to the emergence of increased resistance to standard therapy. However, the entire population of cancer cells within a tumor is not responsible for showing therapeutic resistance; only a small subpopulation within it, the cancer stem cells (CSCs), are. The CSCs show resilience to established anticancer drugs and are responsible for the higher relapse rate of solid tumors. An intimate association was drawn between the expression of several pluripotent marker genes (Oct4, Sox2, Nanog) and the acquisition of chemo-resistance in reprogrammed CSCs. In this regard, the role of Sox2, belonging to the SRY-related HMG box family, was associated with promoting aberrant self-renewal in breast cancer. Leis et al. (2012) revealed that of all pluripotency master regulator genes (Oct4, Sox2, Nanog), only Sox2-positive staining was obtained in the early-stage immunohistochemical specimens of all major breast cancer subtypes. High Sox2 levels in Breast cancer tissues have been correlated with worse prognosis, shorter overall, and disease-free survival in patients. Therefore, it can be said that targeting Sox2 oncogenic activity can be a prospective strategy to overcome the challenges associated with drug resistance and tumor recurrence. At our Cancer Biology Lab at SMST, we have explored the potential of targeting CSC populations in breast cancer with repurposed drugs. Our research group has shown that Sox2 is associated with self-renewal and chemoresistance in breast cancer. We further aim to understand the mode of oncogenic action of Sox2 in facilitating breast cancer progression and design novel therapeutic strategies based on that. We also want to analyze the signaling pathways regulated by Sox2 in breast cancer.