In CRC models, UA induces G2/M arrest and caspase-dependent apoptosis, suppresses Wnt/β-catenin programs, dampens glycolytic flux via p53/TIGAR, and enhances 5-fluorouracil (FU) efficacy while modulating drug transporters [16,17,18,19,20,21]. The gene discussed is TP53; the disease is colorectal carcinoma.