The functionality of C1QA rs292001 and C1QB rs631090 has been previously shown in lupus erythematosus [18]. Nevertheless, our study revealed no association of these two functional variants with schizophrenia. At present, there are no published data on functionality of the C1QB rs291982 and rs913243 polymorphisms. In order to explore possible functional role of these genetic variants, we use the web server ALGGEN, a convenient tool for identification of the functional effects of SNPs [30]. Analysis showed that both C1QB rs291982 and rs913243 SNPs were found to be intronic enhancers. Thus, the C1QB rs291982 minor G allele contains binding sites for transcription factors forkhead box P3 (FOXP3, also known as hepocyte nuclear factor 3 (HNF3), forkhead homologue 2 or HFH-2), progesterone receptor isoform A (PRA) and B (PRB), absent in the T major allele. Further, the rs913243 G/T polymorphism of the C1QB gene leads to loss of binding sites of glucocorticoid receptor-alpha and retinoid × receptor-alpha transcription factors. Whereas these types of functional effects have low phenotypic risk [31], the results of our analysis might indicate the functionality of the C1QB rs291982 and rs913243 SNPs as enhancers, transcription-stimulating DNA regulatory elements [32]. Importantly, these transcription factors might have an indirect impact on the immune system [19–22], therefore, might contribute to the etiology of schizophrenia taken into account immune system alterations in this disease [6–13].