More than 50% of patients with ovarian cancer have genetic alterations in the homologous repair pathway. Trabectedin appears to induce damage more readily in tumor cells with defects in the homologous repair system. Moreover, trabectedin inhibits monocyte differentiation into tumor-associated macrophages and inhibits the production of inflammatory mediators such as IL-6. In patients with platinum-sensitive, relapsed ovarian cancer, trabectedin plus pegylated liposomal doxorubicin was associated with a trend towards improved overall survival by extending the platinum-free interval. These clinical effects could possibly be attributed to actions of trabectedin on the tumor microenvironment (e.g., a reduction of IL-6). Thus, trabectedin is an agent with mechanisms of action especially appropriate for targeting key processes in the biology of ovarian cancer.