The “Th2 hypothesis” for asthma pathogenesis is based on a relative increase in T-helper (Th) type 2 (Th2) cellular responses in combination with a decrease in Th1 re–sponses. The consequent alteration in cytokine milieu (most likely in the lung), with excess Th2 products (eg, interleukin [IL]-4, IL-5, and IL-13) in concert with decreased Th1 products (eg, interferon [IFN]-and IL-12), is predicted to drive the asthma phenotype. Evidence for such a shift in the Th1/Th2 balance derives from studies of asthma in cellular and murine models, where Th cell polarization and allergen-dependence of Th2 responses are most easily defined (1), and from human studies that profile cytokine production (2, 3). As noted previously (4) and again herein, this paradigm may be challenged, but even if correct, the basis for its development (and a consequent strategy to prevent it) remains uncertain. A leading proposal to explain the imbalance toward Th2 responses (and the asthma epidemic) is that developmental stimuli of the Th1 system are lacking in the present compared with past eras. If so, it then becomes natural to propose that increased stimulation of the Th1 system, presumably early in life and selective for the lung, may serve to prevent the Th2 diathesis and resulting atopic diseases such as asthma. All of these possibilities are cogently espoused in the accompanying perspective by von Hertzen and Haahtela (5) as well as other recent reports (6–8). In the current case, the authors combine this point of view with the related need for an improved vaccine for another pressing health problem, ie, tuberculosis. In combination, they suggest that early life induction of a Th1 immune response by vaccination with a better Calmette–Guerin bacillus (BCG)(or other species of Mycobacteria), if strong enough to evoke immune memory, may prevent environmental sensitization to allergens and the development of a Th2-dependent disease such as asthma. In this perspective, we aim to point out some of the “other” issues related to this proposal; first in relation to the development of the immune phenotype, and second, to what happens after the phenotype is developed (eg, during a flare of the disease).