To further elucidate the role of Bmal1 in the occurrence and development of AT, we used small interfering RNAs (siRNAs) to knock down Bmal1 in TDSCs, while utilizing pcDNA3.1(+)-Arntl-3xFLAG vectors to increase the expression of Bmal1. The results of qPCR showed that specific knockdown of Bmal1 led to a reduction in the rhythmic expression amplitudes of Bmal1 and Nrf2, whereas overexpression of Bmal1 resulted in an increase in amplitudes (Fig. 3I-K and Figure S3D). The gene discussed is BMAL1; the disease is ataxia telangiectasia.