The results of our study were as follows: (I) ALDH2 deficiency does not affectthe process of compensatory cardiac hypertrophy induced by CKD, but resulted incardiac dysfunction in this CKD model; (II) ALDH2 deficiency could exacerbateoxidative stress post CKD challenge, as evidenced by increased levels of ROS anddecreased expression of antioxidants, including UCP2 and Nrf2, which might beresponsible for the reduced cardiac function in this model. The gene discussed is ALDH2; the disease is chronic kidney disease.