However, the subsequent effects of Bax and Bcl-2 on the permeability of the mitochondrial outer membrane need to be further confirmed in breast cancer treatment with flubendazole, which leads to the dissipation of mitochondrial membrane potential and provides a channel for the release of mitochondrial intermembrane space proteins (most importantly, Cyto C) [27]. The gene discussed is BAX; the disease is breast carcinoma.