Previous studies have hypothesized that the elevated parasite load and antigenic abundance fuel the inflammatory response, leading to ulcer development109 Thus, the development of the classical ulcer occurs concomitantly with the production of both gamma interferon (IFN‐γ) and tumor necrosis factor‐alpha (TNF‐α), and both positively correlate with lesions size and severity of the disease observed in the patients.110, 111. The gene discussed is TNF; the disease is ulcer disease.