From present results, we safely posit a potential mechanism that over-expressed Bcl-2 binds to Twist1 and that the formation of the Bcl-2/Twist1 complex promotes the transport of two factors into nucleus, which synergistically promotes the transcription of downstream target genes and leading to a cascade of changes in cell phenotype remodeling, migration, invasion and tumor growth. This evidence concerns the gene TWIST1 and neoplasm.