These in vitro data support and extend our in vivo tumor analysis demonstrating decreased nuclear translocation of NF-κB by CR in the pancreatic tumor microenvironment, and more specifically, that IGF-1 (at levels approximating those found in overweight/obese mice) activated NF-κB and increased transcription of genes associated with several hallmarks of cancer development. The gene discussed is NFKB1; the disease is cancer.