NF-κB is constitutively activated in many types of cancer and activated NF-κB can have critical roles in the progression of cancer through regulation of cell survival, apoptosis, and drug resistance.25, 26 It was recently reported that the interaction between alternatively spliced segments of tenascin-C and ANXA2 on the cell surface of pancreatic cancer cells induces gemcitabine resistance through canonical PI3K/Akt/NF-κB signaling pathways,27 although the precise mechanism by which ANXA2 and tenascin-C interact to affect gemcitabine resistance is unknown. This evidence concerns the gene AKT1 and cancer.