Interesting results were also obtained in cervical cancer cells with the use of niclosamide, which could improve the response to paclitaxel treatment by inhibiting mitochondrial respiration, complex I activity, and ATP secretion, thus, leading to mitochondrial dysfunction and oxidative stress, and the consequential impairment of the mammalian target of the rapamycin (mTOR) signaling pathway [75]. This evidence concerns the gene MTOR and cervical cancer.