The treatment mechanism of Schottky heterojunction for AT can be attributed to the “triple hit” approach: (I) enhancing the expression of Bmal1 and Nrf2 to bolster the body's antioxidant and anti-inflammatory defense mechanism; (II) increasing the amplitude of rhythmic expression of Bmal1 and Nrf2 to restore stable circuitry and clock output; and (III) directly adsorbing and scavenging ROS to mitigate ROS-induced oxidative stress damage. This evidence concerns the gene NFE2L2 and ataxia telangiectasia.