We studied the reading performance of 340 consecutive, Italian-speaking aphasics in order to evaluate the clinical features of deep dyslexia, the functional impairments underlying semantic paralexias, and their neuranatomical correlates. Semantic paralexias were observed in 9/340 subjects (2.4%). Our data and a review of the literature show that most deep dyslexics suffer from superficial and deep vascular damage in the territory of the left middle cerebral artery, and that they are relatively young, well-educated individuals, in the chronic stage of their disease. In these subjects, perisylvian damage might be mainly responsible for damage to sublexical grapheme–phoneme Conversion (GPC) procedures, and extrasylvian damage for lexical–semantic impairment. Semantic paralexias might originate in the right hemisphere, or in left perilesional regions. The functional impairment underlying deep dyslexia was analyzed with specific reference to the summation hypothesis, i.e., to the hypothesis that in reading, GPC procedures interact with lexical–semantic information, thus blocking semantically incorrect responses. On this account, semantic paralexias should only occur when, in the presence of lexical–semantic damage, GPC rules are disrupted to the point that the interaction can no longer take place. In agreement with the hypothesis, only cases with co-occurring lexical–semantic and GPC damage produced semantic paralexias; and, these were the subjects with the most severe GPC damage. The inability to apply approximately 45% GPC mappings is the critical level of sublexical damage that no longer allows GPC procedures to interact with lexical–semantic information.