Studies have revealed that patients with GERD exhibit distinct bacterial abundance compared to healthy individuals, accompanied by significantly elevated levels of certain proinflammatory cytokines, including interleukin-4, interleukin-1β, and tumor necrosis factor-α.[39,40] Additionally, in patients with GERD, an increased abundance of gram-negative bacilli has been observed, which leads to an upregulation of inflammatory cytokines such as interleukin-18, tumor necrosis factor-α, and cyclooxygenase-2. The gene discussed is IL18; the disease is gastroesophageal reflux disease.