These findings suggested that ATO-mediated induction of oxidative stress suppressed miR-182-5p, leading to the up-regulation of SESN2. A cytotoxicity assay showed that transfection of a miR-182 mimic into S1 GBM cells substantially enhanced the cytotoxic effect of ATO at higher concentrations (Figure 1H). The gene discussed is SESN2; the disease is glioblastoma.