Before one gets too excited about the potential of these data to illuminate a mechanism for cyclic pathologic mood states in bipolar disorders, it is important to note that the literature, particularly with regard to depressed bipolar I disorder, is decidedly mixed at the moment, with some studies finding increased, others decreased, and yet others no significant change in amygdala reactivity (12). There are many likely contributors to this heterogeneity, including studies that 1) collapse patients in manic, depressed, and euthymic states, 2) focus on medicated or nonmedicated patients, and 3) use a variety of experimental paradigms. A notable methodological strength of the research conducted by Altshuler's team is the use of the same functional task paradigm in all of their studies, which has facilitated cross-sectional comparisons across mood states in bipolar I and II disorders. Longitudinal research within a cohort of patients is now necessary to identify the neural basis of the transition between states and the triggers for these transitions. In this context, it will be interesting to establish how observed changes in corticolimbic circuitry map onto specific dimensional aspects of dysfunction, an element missing from the current research.