ulation of IgE biosynthesis, IL-5, IL-3, and GM-CSF stimulate proliferation and maturation of eosinophils. GM-CSF, rather than IL-3 or IL-5, has been described as associated with eosinophil survival–enhancing activity in asthmatic subjects.2 In addition, GM-CSF has been shown to assist eosinophil adhesion to vascular cell adhesion molecule-1 and eosinophil migration into tissues, a characteristic of allergic diseases.3 It also stimulates the maturation of antigen-presenting cells. However, the expression of GM-CSF, a 4 α-helix glycoprotein, seems to be increased in atopic subjects with asthma compared with control subjects.4 Thus although previous research with the candidate gene approach has concentrated on IL-4 and IL-5, GM-CSF represents an encouraging candidate gene for atopic asthma. We investigated whether any sequence polymorphisms in the 4 exons of the gene for GM-CSF were associated either with IgE or BHR in asthmatic children compared with control subjects. Asthma is a phenotypically heterogeneous inflammatory disorder clinically characterized by reversible airway obstruction. Atopy, the production of a sustained high-level IgE response to common environmental allergens, and bronchial hyperresponsiveness (BHR) are commonly found in asthmatic subjects. Both asthma and atopy are based on strong genetic components inherited in a complex pattern. Evidence for linkage between asthma and atopy and markers in the IL-4 cytokine gene cluster on chromosome 5q31-q33 have been reported.1 The proinflammatory cytokines (IL-3, IL-4, IL-5, IL-9, IL13, and GM-CSF) encoded on 5q31-33 are expressed by TH2 cells orchestrating the allergic inflammatory response. Although IL-4 and IL-13 are likely to be involved in IgM-to-IgE isotype switching and the upregAbbreviation used BHR: Bronchial hyperresponsiveness