Giant cell arteritis (GCA) affects middle-sized or large arteries in individuals over 50 years of age. GCA is characterized by a combination of focal inflammation responsible for arterial stenosis or occlusion and of systemic inflammation manifesting as polymyalgia rheumatica, a decline in general health, and inflammatory anemia. In addition to the typical involvement of the branches of the external carotid arteries, relatively common sites of involvement include the aorta, most notably in its thoracic segment, and the subclavian, axillary, brachial, vertebral, and femoral arteries. The treatment of GCA rests on daily glucocorticoid administration, which should be started on an emergency basis in patients with incipient visual impairments (diplopia or amaurosis fugax). The duration of glucocorticoid therapy is unpredictable and side effects are common. Initial megadose glucocorticoid therapy does not decrease subsequent glucocorticoid requirements. Glucocorticoid therapy regulates the Th17 pathway, which is involved in the prominent vascular and systemic manifestations; but not the Th1 pathway, which may underlie the chronic course of the disease (whereas aspirin, in addition to decreasing platelet aggregation, blocks the Th1 mediator interferon-gamma). Although GCA is classically described as resolving within 1 to 3 years, clinical practice often teaches otherwise. Many patients experience rebound abnormalities in laboratory tests and/or relapses, and some of them have recurrences after an apparently full recovery. Histological documentation is useful to confirm the diagnosis. The effect of methotrexate and TNFα antagonists is modest at best. A few patients have responded to tocilizumab, which suppresses IL-6, a key cytokine in GCA. Life expectancy in GCA patients is similar to that in same-age controls except for a slight excess in vascular mortality shortly after the diagnosis.