In GC, the de-regulation of p16 has been shown to significantly increase the risk of malignant transformation of gastric epithelial cells21, and the silencing of INK4 members induced by Ras homolog family member A (RhoA) has been associated with G1/S progression, indicating that INK4 members are involved in GC cell proliferation22. The gene discussed is CDKN2A; the disease is gastric cancer.