Psychopathy is a developmental disorder marked by emotional hypo-responsiveness and an increased risk for instrumental and reactive aggression. In this paper, it will be argued that the developmental origins of psychopathy do not lie in orbitofrontal cortex (OFC) dysfunction. This is because the key functional impairments seen in psychopathy are associated with amygdala damage, not with OFC damage. However, it will be argued that the role played by the integrated functioning of the amygdala and medial OFC in stimulus-reinforcement learning and decision making is disrupted in psychopathy. Impaired learning of stimulus-reinforcement associations and representation of reinforcement expectations are thought to underlie the impairments in socialization and appropriate decision making seen in psychopathy. It is suggested that the impairment in the role of medial OFC in prediction error signaling and the detection of contingency change may underlie the impairments in flexible behavioral change seen in psychopathy.