In ovarian cancer, resistance is driven by overexpression of DNA repair proteins (e.g., BRCA1/2, RAD51), epigenetic alterations, and a hostile tumor microenvironment (TME) characterized by cancer-associated fibroblasts (CAFs), tumor-associated macrophages (TAMs), and extracellular matrix (ECM) remodeling [31]. Here, RAD51 is linked to neoplasm.