These findings partially correlated to previous studies of Donia et al. [16], who suggested that Hesp exerted antitumor properties and possessed an ameliorative effect against doxorubicin cytotoxicity, while enhancing its antitumor effect, attributing this to the ability of Hesp to arrest tumor growth via the apoptotic pathway by downregulating the expression of Bcl-2, an antiapoptotic gene, and upregulating the expression of the Caspase3 and Bax genes, apoptotic genes. The gene discussed is BAX; the disease is neoplasm.