In the present study, we demonstrated that the ARS analogue ART could inhibit glioma malignancy through two mechanisms: (a) inhibiting the nuclear localization of SREBP2 and its target gene HMGCR, which have been demonstrated to be oncogenes, and (b) disrupting the interaction between SREBP2 and P53, which up‐regulated P21 expression and induced senescence (Figure 6). The gene discussed is TP53; the disease is glioma.