Triple-negative breast cancer (TNBC) is a complex heterogeneous disease that lacks the expressions of hormone receptors (HR) and human epidermal growth factor receptor 2 (HER2). Although TNBC make up less than 20% of breast cancer, it accounts for a large number of metastatic cases and deaths. Currently, extensive efforts have been made to look for potentially biomolecular targets for TNBC treatment. Based on the differences of molecular events identified by gene profiling analysis, the TNBC may be divided into some broad categories: basal-like (BL), mesenchymal-like (ML), immune-associated, HER2-enriched and luminal/apocrine breast cancers. Most of these are in the BL-TNBC category. BL-TNBC carries a representative molecular event of DNA-repair deficiency that increases the effectiveness of DNA destabilizers (represented by platinum agents) and DNA-damage response inhibitors (represented by PARP inhibitors). However, the results from clinical and preclinical studies have been inconsistent. Herein, we simply outline the progress of breast cancer classification and the significance of DNA repair deficiency in the clinic treatment for TNBCs. Previous studies have shown that the neoadjuvant therapies with platinum agents are effective for early-stage and metastatic TNBC patients with DNA repair defects. The results indicate that proper biomarkers (such as homologous recombination repair defects, HRD) are necessary for predicting the response to chemotherapy and often sufficient to select patients in early-phase treatment. Furthermore, the combination of chemotherapy drugs and inhibitors of DNA damage response represents a potential therapeutic strategy for TNBCs.