The selection of A498 cells was informed by prior evidence demonstrating their responsiveness to 5-Aza-CdR-mediated demethylation and reactivation of tumor suppressor genes (e.g., WNT7A, KRT19, BTG3) [25, 26], confirming sufficient endogenous DNMT activity for pharmacological inhibition. The gene discussed is DNMT1; the disease is neoplasm.