This work[33,34] was groundbreaking in identifying NO-mediated resistance to PDT in vivo, but it left many important questions unanswered, including: (1) the cellular source(s) of resistance-enhancing NO, e.g., tumor cells themselves, vascular endothelial cells, macrophages, or all of these; (2) which NOS isoform was the major source of resistance NO; (3) whether the NOS in question acted at a basal (constitutive) level or at a stress-induced level; and (4) the underlying mechanism(s) of NO-mediated resistance. This evidence concerns the gene NOS1 and neoplasm.