Biological agents have originally been developed to treat refractory arthritis, but evidence has been accruing, supporting their use in vasculitis as well. In the large-vessel vasculitides giant cell arteritis and Takayasu arteritis, TNF-α inhibitors have shown some efficacy in patients with relapsing disease. In contrast, in patients with recent onset of giant cell arteritis, TNF-α inhibitors failed to provide a significant benefit over and above that conferred by glucocorticoids alone. More recent, preliminary data suggest a role for the interleukin-6 receptor antagonist tocilizumab in both resistant and treatment-naïve giant cell arteritis and Takayasu arteritis. Biological agents have also been proposed to treat difficult anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis. Uncontrolled observations suggest that the TNF-α inhibitor infliximab might be beneficial in resistant cases. On the contrary, a randomized controlled trial did not show superiority of the recombinant human soluble TNF-α p75 receptor fusion protein etanercept over placebo in maintaining remission in granulomatosis with polyangiitis. Two randomized controlled trials have demonstrated that the anti-CD20 monoclonal antibody rituximab was as effective as the standard-of-care agent cyclophosphamide in inducing remission. In addition, rituximab appeared to be superior to cyclophosphamide in inducing remission in the subset of patients with relapsing disease. These findings prove that biological therapy has a role in vasculitis. Research is investigating novel therapies as well as focusing on how to best use the available drugs.