The fear is one of the strongest emotions that drive our behavior. And the amygdala is the central hub for processing the fear responses. How would our life be changed if we were to lose both of the amygdalae? While the animals can be deprived of fear by knocking out Stathmin, a cytoskeleton regulatory protein concentrated in the amygdala and other parts of the fear circuit, these animals cannot report on their internal subjective experience. Unfortunately, no drug is presently safe enough for a temporary amygdala inactivation in humans. Our understanding of a human condition without the amygdalae has been, therefore, rather limited, relying on a handful of patients with a rare genetic disorder, the Urbach-Wiethe disease, which produces bilateral calcifications on the medial temporal lobes, ultimately leading to a destruction of the amygdalae. One of these patients, a woman called S.M., has been studied extensively since 1994 and provided the wealth of psychological and neurological information about her condition. During the course of an extensive psychological evaluation, she reported feeling upset, angry, and irritable, but on no occasion did S.M. experience any fear, guilt, or shame, induced either by real-life experiences (being held up at knife point and at gun point) or by unpleasant thoughts (e.g. about dying). These findings suggest that because of her amygdala damage, S.M. became immune to the devastating effects of posttraumatic stress disorder (PTSD). Similarly to S.M., the Vietnam War veterans with considerable damage to the amygdala have a lower occurrence of PTSD, as described in this Nature Neuroscience 2007 paper. Moreover, when PTSD patients are provoked to recall their traumatic memories, they exhibit an increased activity in the amygdala and the head of the caudate nucleus, as reported in this recent fMRI study. Overall, there is a considerable body of knowledge suggesting that the amygdala inactivation, perhaps through chronic neuromodulation, could be an effective method for PTSD treatment.