OBJECTIVE： To utilize CYP2C19， ABCB1 and PON1 gene testing so as to guide individualized administration of clopidogrel in ischemic stroke patients. METHODS： Totally 23 patients with ischemic stroke were collected from our hospital during Nov.-Dec.， 2016. Genotype of clopidogrel related gene （CYP2C19*17， CYP2C19*3， CYP2C19*2， ABCB1 and PON1） were determined by Sanger sequencing method. Clinical pharmacists provide suggestions according to genotype. A patient with recurrent ischemic stroke was collected. Inhibitory rate of clopidogrel， intensity of blood clot formation （MA） and the genotype of above clopidogrel related gene were determined. The suggestions about individualized anti-platelet therapy were provided for patients. RESULTS： Among 23 patients， CYP2C19*17 was wild type of CC； among which CYP2C19*3 testing results were one person had mutant heterozygous type of AG； CYP2C19*2 testing result showed that 10 persons had mutant heterozygous type of AG， which were intermediate metabolic type； CYP2C19*2 testing result showed that 3 persons had mutation homozygous type of AA， which were slow metabolic type. 14 patients above were suggested to stop using clopidogrel. The remaining 9 patients were normal metabolic type， among which there was no mutant homozygous type of ABCB1 gene， and 6 persons were PON1 gene mutation type. It was recommended to take clopidogrel at normal dose. Inhibitory rate of clopidogrel was 0 in 2 times of testing for a patient with recurrent ischemic stroke， MA were 66.4 and 68 mm， ABCB1 was mutant heterozygous type， and drug absorption slowed down； CYP2C19*2 was mutant heterozygous type， PON1 was mutant heterozygous type. It was suggested that clopidogrel should be stopped by the reduction of enzyme activity and slowing down of drug metabolism. CONCLUSIONS： Gene detection guide individualized administration of clopidogrel in ischemic stroke patients so as to achieve secondary prevention of stroke and reduce waste of medical resources.