Reduced prefrontal regulation of emotion, were less likely than L-carriers to endorse saving many lives if one person would be unintentionally harmed as a result. LL genotype participants judged foreseen harm to be more acceptable, and they responded more slowly when judging foreseen harm to be unacceptable, suggesting increased response conflict in these trials. These high levels infection findings support our hypothesis that LL genotype participants�� moral judgments are more strongly modulated by assessments of intentionality. These results may aid in understanding why people disagree about the acceptability of causing foreseen harm to meet utilitarian goals. The results of the present study suggest that judgments in response to this kind of moral dilemma may be influenced by inherited variants in a genetic polymorphism that influences serotonin neurotransmission and patterns of responding to socioemotional stimuli. These findings thus extend previous research in two domains. First, they advance our understanding of how variations of the 5-HTTLPR influence social cognition. Second, they indicate that a genetic ����manipulation���� consistently associated with increased emotional responsiveness results in significantly greater reluctance to cause harm to another individual even though others will be helped, and even though harming the innocent is an unintentional aspect of helping. This helps to extend our understanding of the mechanisms underlying moral judgments. Serotonin function has long been associated with variations in personality and in patterns of affective responding. 5HTTLPR S-carriers have been characterized as high in negative affectivity, which is defined as a bias toward negatively valenced information and sensitivity to perceived threat. The results of neuroimaging studies suggest that this pattern of responding results from enhanced reactivity of the amygdala to negatively valenced stimuli and/or reduced modulation of this activity by the prefrontal cortex. In the present paradigm, we speculate that these patterns of neural responding, and consequent increased emotional responsiveness, are reflected in S-carriers�� reluctance to condone even unintentional harm to an innocent victim despite the possibility of utilitarian gains. To draw stronger conclusions about the mechanism by which genotype affects moral judgments, it would be optimal to specifically assess correlates of affective responding during moral judgments in S and L-carriers, for example, via psychophysiological or self-report measures of affective responding. Such paradigms could provide support for the notion that the prospect of harming an innocent victim generates an aversive emotional response, one that may be enhanced in S-carriers. Neuroimaging studies of the amygdala and prefrontal cortex in S and Lcarriers could also test the hypothesis that harming innocents will generate increased amygdala responses in S-carriers relative to LLhomozygotes��particularly in response to unintentional but foreseen harm scenarios. It should be noted that the patterns of response times we observed suggested that LL homozygotes experienced increased response conflict when their responses contradicted the doctrine of double effect, whereas S-carriers did not show consistent differences in response time across conditions. Previous research has demonstrated that when participants judge harming an innocent victim to be acceptable their response latencies are usually slower than when they judge these items to be unacceptable.