To determine whether Schottky heterojunction could be used as a therapeutic approach to treat AT by enhancing Bmal1 expression, we evaluated its effects on the stimulation of Nrf2: luc activity, and the luciferase assay results indicated that the overexpression of Bmal1 in TDSCs led to a significant stimulation of Nrf2: luc activity, and this increase was further enhanced by Schottky heterojunction treatment (Fig. 5A). This evidence concerns the gene BMAL1 and ataxia telangiectasia.