In conclusion, our findings indicate that in breast cancer cells, in response to cambogin treatment, the NOX enzyme is activated through the enhancement of p22phox and NOX1 interaction, and ROS derived from NOX stimulation subsequently leads to the dissociation of Trx1 from ASK1, resulting in the activation of ASK1/JNK pathway and the induction of mitochondrial network abnormalities, leading to the inhibition of breast adenocarcinoma cell proliferation and ultimately cell death. This evidence concerns the gene NOX1 and breast adenocarcinoma.