Introduction: Schizophrenia (SZ) is a neurological disorder, the causative agents of which may be multiple factors like genetic, environmental factors, or co-morbidities with other diseases. The actual reason for the occurrence of this disorder is yet to be unrevealed. The genes responsible for this disorder are vulnerable to mutations at the chromosomal or protein levels. So identification of disease-associated mutations may pave the way for divulging the root cause behind the disorder. In the current study, the emphasis had been made on finding the said disease-associated mutations for the disorder through in-silico analyses. Methods: The genes and FDA approved antipsychotics were prioritized using text mining approach, which shortlists nine genes (COMT, DISC1, DAOA, NRG1, PRODH, RGS4, GRM3, DRD3 and DTNBP1) and seven antipsychotics (Haloperidol, Fluphenazine, Aripiprazole, Clozapine, Iloperidone, Lurasidone, and Risperidone). The genes were checked for deleterious or damaging mutations using SIFT and PolyPhen servers. Results: The SNPs rs6267 and rs4986871in COMT protein were found deleterious with both the servers. SNPs rs2391191 and rs9558562 were found damaging in DAOA protein. In case of DISC1 protein five SNPs (rs6675281, rs821616, rs3738400, rs34622148, and rs55795950) were found damaging. NRG1 and RGS4 protein have one deleterious mutation (rs3924999 and rs68678746 respectively) and three deleterious mutations (rs450046, rs2870984 and rs397055) were present in PRODH protein. The SNPs rs181422088 (in DRD3) and rs16876589 (in DTNBP1) were found deleterious with both the servers. The native protein and their mutated form were modelled and docked with the antipsychotics to check their binding energies. Conclusion: The results showed that the binding energies between antipsychotics and mutated proteins were lower as compared to native protein suggesting that mutated proteins bind well and were stable, so a person is prescribed antipsychotics to reduce the symptoms of the disorder. Thus, these mutations may be the reason behind the pathophysiology of the disorder.