These include excessive activation of the NF‐κB pathway, resulting in elevated levels of pro‐inflammatory cytokines such as IL‐1β, IL‐6, IFN‐γ, and TNFα,119 as well as an increased recruitment of myeloid‐derived suppressor cells to the gastric epithelium where they suppress the host's anti‐tumor immune response.120 IL‐1β has also been shown to promote gastric atrophy by suppressing Sonic hedgehog gene expression in parietal cells, resulting in decreased acid secretion and release of intracellular calcium.121. Here, IL1B is linked to chronic atrophic gastritis.