From our results, we concluded that DENA/AAF administration downregulated the Bax/Bcl-2 ratio by increasing the cell proliferation rate; this result agrees with those of Harandi et al. [60], who suggested that a higher Bax/Bcl-2 ratio results in tumor hypersensitivity to drugs, and an increase in the ratio suggests increased cellular death. The gene discussed is BAX; the disease is neoplasm.