We have previously reported that bactofection of plasmids encoding a peptide from the BH3 domain of the proapoptotic Bax protein, antagonized the antiapoptotic activity of the Bcl-2 family proteins, restored apoptosis, and induced chemosensitization of tumor cells [29], and we have recently documented that a cell-permeable Bax BH3 peptide expressed and released into the tumor microenvironment via a live-attenuated bacterial vector promoted apoptosis, induced antitumor activity, and increased survival in a murine xenograft model of human B non-Hodgkin's lymphoma [30]. Here, BAX is linked to neoplasm.