Triple-negative breast cancer (TNBC) is still one of the most enigmatic breast cancer types and no firm, efficient therapy has been established yet. Regarding its molecular profile and lack of specific receptors, angiogenesis, as an inseparable part of tumor biology, was taken into consideration as one of the leading causes of tumor progression. Taking into account cancerous neovascularization stages and recent scientific researches, it appears probable to understand the process of tumor progression and separate several ways of inhibiting this crucial phenomenon determining neoplasm invasiveness. Combination of traditional therapy and new antiangiogenic agents is a chance for patients to receive treatment as effective as patients with other types of breast cancer or cancer at all. New therapeutic methods may impact the genome level of carcinogenesis. There are many studies aimed at blocking transformed protooncogenes or restore the activity of tumor suppressor genes. Dealing with the process of cancer cells hypoxia and understanding the role of hypoxia inducible factor (HIF) and vascular endothelial growth factor (VEGF) – main angiogenesis inducers – let us introduce proper drugs blocking their activity (e.g. indenopyrazole 21, bevacizumab). Monoclonal antibodies, genetic therapies and newly synthesized drugs replace previously used therapeutic methods as poly (ADP-ribose) polymerase (PARP) inhibitors, mTOR kinase inhibitors, or Ras inhibitors. These new treatment methods include sunitinib, Aurora A kinase/tyrosine kinase inhibitor ENMD-2076, tested due to their multi-target actions, oncolytic viral therapy or small interfering RNA (siRNA). Despite numerous scientific and clinical studies, triple-negative breast cancer remains difficult to treat and is characterized by significantly worse prognosis, statistically shorter five-year survival rate and tendency to relapse.