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Various lifestyle and environmental exposures have been suggested as risk factors for childhood asthma development. However, the evidence on atopic and non-atopic asthma phenotypes has been limited.1 The word atopic here refers specifically to IgE-mediated immune system over-reaction to common allergens, as detected by skin prick tests (also known as allergic asthma), rather than genetic predisposition (ie, inherent tendency) to develop allergic conditions. Because different underlying pathophysiology may require distinct preventive measures and treatment strategies, it is important to explore asthma phenotypes and endotypes, rather than treating asthma as a single, homogeneous condition. However, the inconsistent definitions of asthma subtypes have resulted in substantial heterogeneity in study findings.1