An emerging theme is that bladder tumors effectively co-opt age-related epigenetic processes to their advantage–for instance, silencing senescence regulators (such as p16-INK4A and miR-34a), upregulating immune-suppressive factors (like EZH2 and HOTAIR), and exploiting the chronic inflammatory microenvironment of aged tissues (Balaraman et al., 2025; Nutt et al., 2020). This evidence concerns the gene CDKN2A and urinary bladder neoplasm.