In this study, STAT3 was also identified as S-nitrosylated protein in the context of pancreatic cancer, and NOS inhibitor caused decreased STAT3 S-nitrosylation and elevated STAT3 phosphorylation and pancreatic cancer cell viability, which is consistent with previous reports of STAT3 S-nitrosylation in other diseases49–51 and highlighted the roles of STAT3 S-nitrosylation in tumorigenesis. This evidence concerns the gene NOS1 and pancreatic neoplasm.