The adaptative response of tumor cells to PDT-generated oxidative stress (i.e., increased NO) correlates with inhibition of the pro-apoptotic role of MAPK/JNK/p38α pathway (100, 114), with consequent downregulation of the anti-apoptotic proteins survivin, BCL-2, and BCL-xL, lessening the caspase-dependent apoptosis (117, 122). Here, BCL2 is linked to neoplasm.