Background & Objective: Neuroinflammation has been proposed as a major mechanism in schizophrenic disorder. Specifically, an increase in the inflammatory response in the central nervous system is capable of activating microglial cells, leading to the release of pro-inflammatory cytokines and thus activating apoptotic signaling. An increase in apoptosis may underlie a potential role of immune neuropathology in the etiopathogenesis of schizophrenia and specifically, the onset of the disorder. We analyzed in whole blood, levels of S100B, the receptor for advanced glycation end products (RAGE) and the apoptotic marker Fas Ligand in a sample of 13 first episode of schizophrenia twice at baseline before the initiation of any antipsychotic medication (A) and 6 weeks later following an antipsychotic monotherapy with olanzapine (B) and in a sample of 10 healthy controls. The S100B, RAGE and Fas Ligand showed statistically significant differences before and after treatment; the S100B measurements yielded a p-value of 0.004 while the soluble RAGE and Fas Ligand measurements yielded a p=0.03, and p=0.04 respectively. The differences between cases and controls were not statistically significant for all measurements, with the only exception being the S100B values where both samples A and B showed significantly higher values than the controls with p=8.5x10-8 and p=2.9x10-10 respectively. Conclusion: The levels of S100B, RAGE, and Fas Ligand of drug-naive first episode psychosis patients with schizophrenia were significantly higher than that of the same medicated first episode psychosis patients, indicating that an increase of apoptotic signaling is present at the onset of schizophrenia and is also associated with treatment progress.