Our previous report indicated BDA-366 (a small-molecule Bcl2-BH4 domain antagonist) could bind to the BH4 domain and induce conformational changes in the exposure of the BH3 domain and abrogate the anti-apoptotic function of Bcl-2 through enhancing the Bcl-2/Bax interaction and further result in inducing Bcl-2-dependent Bax activation and mitochondrial dysfunction, and inhibiting Bcl-2/IP3R interaction and further inducing Ca2+ release in lung cancer cells [36]. Here, BAX is linked to lung carcinoma.