Schizophrenia is a mental disorder characterized by a breakdown in thinking and poor emotional responses. There has been increasing awareness of the prevalence of childhood sexual abuse (CSA) and the psychological damage that this can cause. Prevalence rates of sexual abuse in the general population range from 4.0% to 21.4% in adults and from 3.0% to 33.2% in children. Males who had suffered child sexual abuse were 1.3 times, and abused females 1.5 times, more likely to have been subsequently treated for schizophrenic disorders than the general population. The medical literature has reported that both psychotic and non-psychotic symptoms in schizophrenia are related to childhood trauma (CT). History of childhood abuse and neglect are common in patients with first episode Schizophrenia (FES), and lead more prominent positive symptoms at first admission. In this paper we are going to discuss man who was abused at the age of 15 and after this traumatic event developed psychotic symptoms. A.P. and 28 years old man was abused by his neighbor at age of 16. After the sexual abuse that he experienced he have been agitated, nervous and afraid of something. He had chief complaints of having impaired sleep talking to self-became aggressive and violent. He was socially isolated and refused going to school. He had visual and auditory hallucinations. He was diagnosed with FES. Several times, he was admitted to EUMF again because of his hallucinations and persecutory delusions that he experienced when he refused taking oral medications. Child abuse and neglect have been found to be causally related to an increased risk of a wide range of psychiatric disorders including anxiety disorders, mood disorders, substance abuse and eating disorders. An association between childhood sexual abuse (CSA) and psychosis was strongly reported in most of the studies. In recent studies, were reported that CT could increase stress sensitivity. It was found that there was a correlation between the cortisol awakening response and childhood sexual abuse and a relationship between CT and decreased BDNF levels in FES patients. It might be possible that CT mediates proneness to psychosis by changing HPA axis and/or by epigenetic processes. Without a long-term prospective study of large numbers of children, who were sexually abused, it is very difficult to be certain whether CSA is an additional risk factor or casual factor in schizophrenia in these children. In conclusion, CSA increases the risk of developing psychotic illnesses and raises the importance of ‘‘asking about childhood trauma when trying to understand or assist people diagnosed with psychosis or schizophrenia’’. It is possible that interventions aimed at preventing CT in children would reduce the manifestation of psychosis among young people.