Allergic march is progression of allergic disorders from atopic dermatitis in infancy to asthma or allergic rhinitis later. Most prospective epidemiologic studies suggest that early atopic dermatitis is a risk factor for the development of asthma, whereas only some subtypes of early atopic dermatitis with concomitant wheeze or less prevalent sensitization were recently reported to be at increased risk of development of asthma during childhood. There is a question as to whether atopic dermatitis itself is a true risk factor for the development of asthma later or allergic march just reflects the order of appearance of atopic dermatitis and asthma or allergic rhinitis. Filaggrin gene mutations are associated with atopic dermatitis as well as asthma with atopic dermatitis in the Western countries, and skin barrier dysfunction can initiate systemic sensitization in the mouse model. Therefore, skin barrier dysfunction can explain partly the mechanism of allergic march. Thymic stromal lymphopoietin and interleukin-17 can also be involved in the development of asthma in the mouse model of allergic march. Moreover, microbial organisms on the skin can enhance or modulate the immunologic mechanism of allergic march. A few pharmacologic agents have been investigated to interrupt allergic march, and the results are not promising. To find effective interruption of allergic march, a well-defined target, further understanding of the mechanism, and development of novel agents or combination of previous agents to modulate immune response remain to be solved.