Additionally, mutations in CTNNB1 exon 3, mainly amino acid substitutions at residues S29, D32, S33, G34, S37, T41, and S45, disrupt key phosphorylation sites, stabilizing β-catenin and thereby activating canonical Wnt/β-catenin signalling pathways that drive cellular proliferation and tumour progression [11]. The gene discussed is CTNNB1; the disease is neoplasm.