It has become apparent that there are many different phenotypic subtypes of asthma. These subtypes are being recognized because patients differ widely in responsiveness to different therapies, in the nature of the inflammatory cell infiltrates that are present in their airways, and in the molecular signature of inflammatory mediators that can be recovered from the airways. Many investigators refer to these subtypes as asthma ‘endotypes.’ The expectation is that classification of patients’ asthmas by endotype will elucidate differences in the underlying pathophysiology of their disease and will improve therapeutic outcomes by permitting their therapy to be matched to the underlying molecular disorder that is leading to symptoms. Some of the most common endotypes include common allergic asthma, exercise-induced asthma, neutrophil-predominant (as opposed to eosinophil-predominant) asthma, and steroid-resistant severe asthma. The fundamental driver of the allergic response in allergic asthma is thought to be pathologically activated TH2 cells, and eosinophils and basophils are prominent in the inflammatory infiltrates in the lungs. In severe, steroid-resistant asthma, TH17 cells appear to play a larger role, and neutrophils are prominent in the inflammatory infiltrates. TH17 cells also appear to be major inducers of the asthmatic syndrome allergic bronchopulmonary aspergillosis (ABPA). Other endotypes are characterized by the participation of additional leukocyte subsets and different effector-cell populations. The endotype of asthma of any individual patient is thought to be the result of the specific conditions under which the individual was sensitized to allergen and the specific predisposition of the individual based on inherited genetic factors and environmentally determined epigenetic factors.