Our recent studies indicate the crucial role of the immune system in schizophrenia and provide evidence on the alterations in the major mediator of the immune response, the complement system, in pathogenesis of this disorder [6–13]. In particular, increased functional activities of the complement classical pathway and C1Q protein, the initiator of the complement classical cascade, in schizophrenia-affected subjects has been found [8, 10]. These findings are of special interest accounting for a positive linkage of schizophrenia with chromosome 1p36 loci located nearby C1QA and C1QB genes (1p36.12) [14, 15]. Notably, for other components of the complement association of genetic polymorphisms with schizophrenia has been demonstrated [11, 16]. In addition association of genetic diversity of HLA-III encoding complement proteins with susceptibility to schizophrenia has been also shown [17]. However, no data regarding association of C1Q encoding genes (C1QA and C1QB) polymorphisms to schizophrenia have been published yet. To explore whether the alterations in C1q activity in schizophrenia are genetically determined or not, in the present study we evaluated the possible association of complement C1Q component gene variants with susceptibility to schizophrenia in Armenian population, focusing on four C1QA and C1QB intronic single nucleotide polymorphisms (SNPs); two tagged SNPs were selected by Martens et al. [2009] using HapMap project [18] and the other two were chosen according to their frequent appearance in European Caucasoid population (minor allele frequency > 10%) and their potential functional effect (gain/loss of binding site for transcription factors) [19–22]. To our knowledge, this is the first study investigating association of the C1QA and C1QB genetic variants with schizophrenia. This study might contribute to understanding the molecular pathomechanisms responsible for generation and development of schizophrenia.