Mice with a C-terminal truncation of Nfkb2 (leading to enhanced DNA binding of RelB/NF-κB2 P52 dimers) develop massive gastric hyperplasia and gastric outlet obstruction.13 There is also in-vitro evidence that H. pylori can enhance NF-κB2 DNA binding in B lymphocytes.14 Hence, a Helicobacter-induced model of gastric carcinogenesis appears to be an ideal model to investigate whether the NF-κB2-mediated signaling influences inflammation-associated carcinogenesis. Here, NFKB2 is linked to hyperplasia.