Studies have shown that GERD does not result from chemical esophagus damage caused by gastric content but rather by cytokine-mediated outcomes.[20,21] CXCL1, a crucial chemokine in inflammation, primarily induces neutrophil recruitment to inflammatory sites.[22] In the human body, CXCL1 acts as an important inflammatory response mediator, inducing neutrophil recruitment and participating in inflammatory responses, potentially leading to tissue damage.[22] The findings indirectly support our results, suggesting that higher predicted levels of CXCL1 may increase the risk of GERD. The gene discussed is CXCL1; the disease is gastroesophageal reflux disease.