CDKN2A generates several transcript variants including p16 and p14ARF. P16 regulates cell cycle by inhibiting CDK4 and CDK6, and thus preventing progression from G1 to S phase. P14ARF acts as a tumor suppressor by inhibiting ribosome biogenesis and initiating p53-dependent cell cycle arrest and apoptosis. Mutations and deletion of CDKN2A are reported in up to 34% of gastric cancer. In addition, EBV-positive gastric adenocarcinoma showed CDKN2A promoter hypermethylation. Gastric cancer with CDKN2A mutations has been shown to be sensitive to CDK4/6 inhibitors in vitro studies. However, predictive or prognostic significance of CDKN2A mutation in gastric cancer is not clear and correlation with other clinical and laboratory findings is necessary. Multiple clinical trials are available for patients with CDKN2A deficient tumors.