We also found that these cells incubated under hypoxic conditions or transfected with pcDNA3.0/HIF-1α under normoxic conditions exhibit heightened NF-κB activity, the inhibition of which results in reversion of the cadherin switch to that of an epithelial phenotype typified by reduced invasion and increased gemcitabine sensitivity, findings that implicate NF-κB as a principal mediator of the HIF-1α-induced EMT program in pancreatic cancer cells under hypoxic conditions. This evidence concerns the gene NFKB1 and pancreatic neoplasm.