In our previous studies, we unveiled a novel insight demonstrating that H. pylori infection activates ACVR1 independently of CagA, thereby promoting the transcriptional activity of CDX2 and initiating intestinal metaplasia.52 Building on these findings, the present study embarks on a comprehensive investigation into the interplay between ACVR1 and gastric cancer pathogenesis. The gene discussed is ACVR1; the disease is gastric cancer.