Schizophrenia is a severe mental disorder that affects approximately 1% of the global population, leading to disability and social deadaptation. One of the main neurobiological mechanisms hypothesized for the disease suggests a defect in glutamatergic neurotransmission. Changes in affinity of glutamate receptors, transcription of their genes, and expression of their subunits in the prefrontal cortex, hippocampus, and thalamus have been revealed in schizophrenics in post mortem studies. Association studies of the genes for kainate and AMPA ionotropic glutamate receptors have yielded discrepant results. In this study, GRIA2 and GRIK2 polymorphisms were tested for association with paranoid schizophrenia (PSZ) and response to haloperidol treatment in Russians and Tatars (257 patients and 349 healthy subjects) from Bashkortostan. Higher PSZ risk was associated with GRIK2*ATG (OR = 3.5) and GRIK2*TGG (OR = 3.12) in Tatars and GRIA2*CCC (OR = 9.60) in Russians. The markers of lower PSZ risk were genotype GRIA2*T/T (rs43025506) (OR = 0.34) in Tatars and GRIA2*CCT (OR = 0.481) in Russians. Genotypes GRIK2*T/T (rs2227281) and GRIA2*C/C in Russians and GRIK2*A/A (rs995640) in Tatars were identified as markers of a low efficacy of haloperidol treatment in improving both negative (NEGAT; flat affect, alogia, and anhedonia) and positive (POSIT; delusions, hallucinations, and disorganized thinking) symptoms. Genotype GRIA2*C/Cy was associated with low efficacy of haloperidol treatment in improving positive symptoms in Russians; such markers were not identified in Tatars. The findings support the hypothesis that glutamate receptor genes are involved in the etiology and pathogenesis of schizophrenia. Interethnic differences in genetic risk factors were observed.