Activated platelets accumulate on ruptured atherosclerotic plaque ulcers， leading to thrombosis. Aspirin is one of the most commonly used antiplatelet aggregation drugs in practice. However， some patients cannot effectively inhibit platelet aggregation after taking aspirin， resulting in aspirin resistance and leading to the recurrence of thrombus events. With the rapid development of molecular biology technology and the human genome project， increasing studies have confirmed that genetic factors play an essential role in thrombus events. Genetic variations can affect platelet function， lead to increased platelet activity， and affect residual platelet aggregation after aspirin treatment. This review provides a further understanding of the genetic factors of aspirin resistance by reviewing domestic and international studies on the role of single nucleotide polymorphisms in aspirin resistance.