By regulating RAD51 and RAD17, miR-506-3p significantly decreases the ability of tumor cells to repair drug-induced DNA damage overall increasing sensitivity to Pt, PARPi and cell cycle checkpoint kinases' inhibitors [(20) and present work.] Such effect strongly suggests a correlation of miR-506-3p expression with EOC BRCAness phenotype particularly for patients with a proficient BRCA status, and support further studies to verify its possible role in predicting response to therapy. The gene discussed is RAD17; the disease is neoplasm.