During the last 100 years, how far has the biological investigation of schizophrenia, its scientific diagnostics, or its modeling progressed? Clinical and/or basic medical studies on schizophrenia, have proposed more than 100 etiologic and pathogenic hypotheses, suggesting the roles of various genes, intestinal bacteria, infectious immunity, and stress exposure, etc. The number of these hypotheses are still increasing and broadening and the confusion of the schizophrenia etiology is rather deepening. One of the reasons stems from the theory of molecular and cellular reductionism as well as from the concept of RDoC. In spite of the theory, the current neuroscience hardly illustrates the integrative system of higher brain function, which performs strong nonlinear processing with multi-variates of sensory inputs and their memory traces. With the limited neuroscience knowledges, therefore, we are not able to fully illustrate any of psychotic symptoms with the current neurosciences. At present, we believe that the selection of the most proper animal model(s) relevant to the schizophrenia pathology or physiology is the most important step. Analysis of the model animal that mimics the cytokine storm famous for COVID-19 and RS virus infection has revealed the possibility that mice or rats exposed to the cytokine EGF may model hallucinations, communication deficits and soliloquy after maturity. The EGF-treated model is known to exhibit similar pathophysiology in various electroencephalogram tests (ASSR, MMN, P300, ABR etc.) as well. Rats seem to have higher intelligence and emotions and perform various games and tricks with human players. Thus we will scientifically reverse-translate the characteristics of the patient's symptomatology and pathophysiology into rodent scales with the modern technology. Such as the fact that the cause of gastric cancer was Helicobacter pylori, we must keep in mind that the biggest problem hidden in academic challenges is the curse of existing concepts and knowledges.
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