Apoptosis is an important cellular event that plays a key role in the therapy of many diseases. The mechanism of the initiation and regulation of photodynamic therapy (PDT)–induced apoptosis is complex. Our previous study found that Photofrin was localized primarily in mitochondria, the primary targets of Photofrin-PDT. The key role of Bax in the mitochondria-mediated apoptosis has been demonstrated in many systems. In order to determine the role of Bax in the mitochondrion-mediated apoptosis induced by Photofrin-PDT, we used the GFP-Bax plasmid to monitor the dynamics of Bax activation after PDT treatment. With laser scanning confocal microscopy, we found that Bax did not translocate from the cytosol to mitochondria when the mitochondrial membrane potential (ΔΨm) disappeared, measured by TMRM. Thus, for Photofrin-PDT, the commitment to cell death is independent of Bax activation.