There is general agreement on the inflammatory pathogenesis of bronchial asthma: an accumulation of activated eosinophils, degranulated mast cells, T lymphocytes and in very severe forms, granulocytes has constantly been found in the bronchial mucosa. In allergic bronchial asthma, inflammation seems to be orchestrated predominantly by a subset of T lymphocytes, with a phenotype similar to the Th2 subset able to produce IL-4 and IL-5. Although corticosteroids are the most potent therapeutic agents used for this disease, their anti-inflammatory effect differs from patient to patient. Some criteria which can be used to define steroid-resistant bronchial asthma are listed here. This review analyzes various molecular alterations responsible for the deficient response to corticosteroid treatment observed in steroid-resistant bronchial asthmatic subjects. New knowledge on the mechanism of steroid resistance may have important implications for the treatment of chronic asthma and other diseases.