Similar to the its role in type 1 diabetes [50], NF-κB increases cellular NO production by the expression of inducible nitric oxide synthase, but downregulates transcription factors (such as Pdx1) associated with differentiation and maintenance of pancreatic β-cell functions (e.g., insulin synthesis and secretion), indicating that activation of the NF-κB pathway may be an important driving force for β-cell dedifferentiation, thereby reducing insulin synthesis and secretion [51]. The gene discussed is INS; the disease is type 1 diabetes mellitus.