We observed in the present study that the expression of MnSOD was upregulated by BTG2 at the transcription level via degradation of IκBα in cancer and normal cells, and that underlying mechanism of APRO effect of BTG2 involved the crosstalk between PI3K-Akt1 and NFκB pathways, which resulted in the scavenge of ROS and increased p21WAF1 expression. The gene discussed is AKT1; the disease is cancer.