Previous reports have discussed the molecular cytotoxicity effects of EOs, and some examples of isolated compounds from EOs towards various cancer cell lines have indicated the mediation of apoptosis, loss of mitochondrial membrane integrity, and several other mechanisms involving the anti-apoptotic factor BCL-2 and pro-apoptotic protein CASPASE-3 [30,31,32,33]. The gene discussed is BCL2; the disease is cancer.