“…This approach has typically led to a large set of mRNAs or proteins being proposed as possible biomarkers in Sz but most findings await replication. Briefly, in a whole blood study from people during their first onset of Sz, the expression of glucose transporter (SLC2A3) and actin assembly factor (DAAM2) were increased, whereas zinc metallopeptidase, neurolysin 1 and myosin C were significantly decreased, compared to controls [129] , indicating peripheral mRNA of these genes could be a potential biomarkers in early stage of disease course. A genomewide expression analysis in PBMC samples from people with Sz was characterized by alterations of genes with immune system function [133,135] with some differentially expressed genes, such as argonaure 2, myocyte enhancer factor 2D, Enah/Vasp-like, peptidase inhibitor 3, S100 calcium binding protein A12 (S100A12), defensin α4 (DEFα4 [133] ) as well as AKT1 [135] being confirmed as changed using qPCR, the result supporting the hypothesis that the disorder has a significant immunological component in its etiology.…”