Consistent with previous observations, we demonstrated that, the expression levels of Bcl-2, Mcl-1 and Bid were downregulated, whereas those of Bax, Bak, Bim, and PUMA were upregulated upon treatment with different concentrations of EM-2, indicating that EM-2 induced apoptosis via the mitochondrial endogenous pathway in LC and BC cells. The gene discussed is MCL1; the disease is breast cancer.