As anti-cancer therapies often target the mitochondrial apoptotic pathway regulated by the Bcl-2 family, overexpression of anti-apoptotic proteins in cancer presents one of the leading challenges to overcome for effective treatment.5 Mechanism of apoptosis induction in cancer is predominantly altered upstream of Bax and Bak.6 Therefore pharmacological suppression of anti-apoptotic Bcl-2 members leading to activation of Bax and Bak should, in principle, be capable of recovering the programmed cell death.7, 8. The gene discussed is BAX; the disease is cancer.