Abnormal activation of ERK can up- regulate the expression of anti-apoptotic members of the Bcl-2 family (such as Bcl-2, Bcl-XL and Mcl-1), especially the expression of the Mcl-1 protein, activates transcription factors, reduce the permeability of mitochondrial membrane, block the release of apoptosis inducing factor (AIF), and interfere with the activity of apoptosis protein mediated by tumor necrosis factor receptor, so as to inhibit apoptosis and promote the survival of tumor cells. This evidence concerns the gene BCL2 and neoplasm.