The relationship between atopic dermatitis (AD) and allergic contact dermatitis (ACD) has long been and continues to be an unsolved and frequently discussed issue. Whereas AD patients have traditionally been considered to have a decreased frequency of ACD, recent studies revealed that these individuals are more or equally likely to develop ACD. The aim of the present review was to determine whether the results of recent experimental studies and theoretical considerations might lead to a parallel shift in our concept on the causal relationship between AD and ACD. It has been shown that Th2 and Th1-type immune responses are not mutually exclusive, and that at least in AD a mixture of both Th2 and Th1 occurs and the interactions between them account for the clinical characteristics of the disease. This new concept on the immunopathomechanism of AD challenges our previous belief that the cytokine pattern of the affected skin is unsuitable for the development of delayed-type hypersensitivity. Since we do not know the exact quantitative balance between Th1 and Th2 reactions along a time axis, we cannot predict whether the cytokine pattern of AD patients favors or inhibits the development of ACD. What we do know with a greater degree of certainty, is that when the eczematous excoriated skin of AD patients, with its defective epidermal barrier (enhancing the penetration of many antigenic substances) is chronically exposed to skin care products and various sensitizing topical medications, it is more likely to develop a superimposed ACD.