Although the earliest iteration of this work [34,35,36] was ground-breaking with regard to PDT antagonism by NO in vivo, it left the following questions unsettled: (i) whether the NO derives from tumor cells alone or whether surrounding cells (endothelial, macrophages, fibroblasts) or tumor-invading, PDT-induced cells like neutrophils might contribute; (ii) which NOS isoform is most important in any given tumor; (iii) whether the NOS/NO in question functions at a pre-existing level or is upregulated by PDT stress; and (iv) the biochemical mechanisms that underlie NO’s anti-PDT effects. Here, NOS2 is linked to neoplasm.