Asthma is an inflammatory disease sensitive to glucocorticoids as has been demonstrated by several studies on the mechanisms of action of these drugs both in vitro and in vivo. The cellular and molecular targets of glucocorticoids have however not been identified. The best candidates are lymphocytes and the glucocorticoid receptors, although other cells and other transcription factors which interact with glucocorticoids may also be involved. Qualitative and quantitative abnormalities in glucocorticoid receptor binding to glucocorticoids and desoxyribonucleic acid have been described in the lymphocytes of patients with corticosteroid-resistant asthma. The chances of observing an abnormality in the mechanism of action of glucocorticoids would be greatest in these patients. Indeed, such deficits might also participate in the pathogenesis of corticosteroid-dependent asthma or in asthma in general. We recall here the mechanisms of action of glucocorticoids and their effect in asthma.