Two key aspects of these studies distinguish them from most others dealing with the pro-tumor effects of iNOS/NO: (1) Rather than simply using unchallenged tumor cells, we applied an oxidative stress-based challenge, viz. PDT, and assessed how it was affected by endogenous iNOS/NO; and (2) We discovered that, in most cases, it was PDT-upregulated iNOS rather than pre-existing (constitutive) enzyme that generated sufficient NO to stimulate resistance and surviving cell aggressiveness. Here, NOS2 is linked to neoplasm.