CContext: schizophrenia is a highly complex syndrome, related to genes, and to non-genetic risk factors. Famous epidemiological studies reported its presence among all cultures and geographic regions. In that sense, Unified Etiological hypothesis face the challenge to both present experimental data, and to show that the findings may cope with the syndrome’s universal profi le. Objectives: systematically review the most prominent Unified Etiological hypothesis, as much as the semantic distribution of genetic findings (under up to date data mining techniques), and propose a new model, based on the dynamic effects of epigenics over genetic activation in both neurodevelopment and early adulthood. Results: in general, Unified Etiological Hypothesis contradict the main genetic findings (which suggest that schizophrenias’ genes are mostly associated with neurotransmitter profiles, like D-1 and the Glutamate-NMDA cascade); also in general, genetic findings are spread all over the genome (as we reveal with a topological map of the 3519 studies on the matter). The key for this conundrum may be represented by the association between the perspective that each polymorphism associated with schizophrenia represents a statistical risk factor (e.g. increasing the risk of developmental instability) while epigenetic molecular cascades and environmental factors considerably influence this picture, affecting genetic activation within critical periods