Semantic cognition permits us to bring meaning to our verbal and nonverbal experiences and to generate context- and time-appropriate behavior [1-2]. It is core to language and nonverbal skilled behaviors and, when impaired after brain damage, it generates significant disability . A fundamental neuroscience question is, therefore, how does the brain code and generate semantic cognition? Historical and some contemporary theories emphasize that conceptualization stems from the joint action of modality-specific association cortices (the "distributed" theory) [4, 5] reflecting our accumulated verbal, motor, and sensory experiences. Parallel studies of semantic dementia, rTMS in normal participants, and neuroimaging indicate that the anterior temporal lobe (ATL) plays a crucial and necessary role in conceptualization by merging experience into an amodal semantic representation [1, 2, 6-8]. Some contemporary computational models suggest that concepts reflect a hub-and-spoke combination of information-modality-specific association areas support sensory, verbal, and motor sources (the spokes) while anterior temporal lobes act as an amodal hub. We demonstrate novel and striking evidence in favor of this hypothesis by applying rTMS to normal participants: ATL stimulation generates a category-general impairment whereas IPL stimulation induces a category-specific deficit for man-made objects, reflecting the coding of praxis in this neural region. © 2010 Elsevier Ltd. All rights reserved.