In contrast, NOS2 is inducible, becomes increasingly expressed in response to inflammation, and produces high levels of NO in a calcium-independent manner.7 Thus, the existing evidence suggests that NOS1 and NOS3 mainly function in promoting tumor development, while depending on the state of a cell, NOS2 might also play an additional role in tumor progression, However, it remains unknown whether distinct NOS isoforms play different roles in regulating autophagy, and which signaling pathways are involved. This evidence concerns the gene NOS3 and neoplasm.