The central brain structure in the circuitry underlying fear conditioning and the perception of threatening stimuli in the environment is the amygdala (4). Deficient amygdala function has been proposed to render individuals unable to recognize cues that signal threat, making them relatively fearless (5). Less sensitive to any negative consequences of their behavior, fearless individuals engage more readily in antisocial behavior. Indeed, the relationship between antisocial behavior and amygdala dysfunction is supported by a number of findings in adults and adolescents, including deficits in recognizing fearful facial expressions, poor fear conditioning, and reduced amygdala responses to negative emotional stimuli as measured with functional neuroimaging (2, 5, 6). While such findings in adults and adolescents are ambiguous as to whether they represent cause or consequence of repetitive antisocial behavior, the results reported here by Gao et al. now point to an early deficit in amygdala function as a causal mechanism. However, the notion of a generally hyporesponsive amygdala would be too simplistic. The amygdala is a small yet complex structure comprising a number of subnuclei with distinct functional properties (4). Moreover, some studies have shown increased amygdala responsiveness in antisocial individuals (2) and in those with a genetic predisposition to aggressive behavior (7). Contrasting with the fearlessness hypothesis outlined above, such findings point to a different pathomechanism whereby pathological aggression may be related to heightened anxiety. Increased amygdala responsiveness is a well-established finding in anxiety disorders and is thought to be the basis for exaggerated fear conditioning. This is nicely demonstrated by another study published in this issue. Using a simple but elegant modification of classical fear conditioning, Lissek et al. (8) show that in panic disorder fear responses are more easily generalized—that is, fear responses are evoked more easily by stimuli that resemble the conditioned stimuli in patients with panic disorder compared with healthy individuals.