Taken together, these results indicate that pharmacological models of schizophrenia that model dopaminergic- (amphetamine) or glutamatergic-related (ketamine) pathophysiological events or neurodevelopmental immunological challenges (LPS or Poly I:C respectively) do not recapitulate the changes on WDFY1 protein levels observed in He–/– mice and schizophrenic patients. The gene discussed is WDFY1; the disease is schizophrenia.