We found that EA in combination with radiation: (a) stimulated ROS generation and inhibited proliferation of HepG2 cells by decreasing p-Akt level; (b) activated the mitochondrial death pathway associated with loss of ΔΨm, caspase-3 activation, higher Bax/BCL2 ratio.; (c) decreased p-Akt, p-NF-κB and p-STAT3 levels in cancer cells; (d) activated p53 and p21; (e) inhibited the onset of secondary survival pathway by decreasing IL-6, COX-2 expression and (f) prevented angiogenesis marker MMP-9 expression. Here, BCL2 is linked to cancer.