GC poses a serious public threat to human health globally, and screening the therapeutic targets for GC is crucial.[1, 3] Previous and our studies showed that m6A RNA modification is involved in pathogenesis and progression of GC.[24, 25] hnRNPA2B1 as an m6A reader promotes tumor development and progression in a m6A‐dependent manner.[26, 27] In this study, we discovered a novel mechanism by which H. pylori‐enhanced hnRNPA2B1 coordinated with PABAC1 to promote mRNA translation and GC progression independent of m6A modification. The gene discussed is HNRNPA2B1; the disease is neoplasm.