Recent breakthroughs have unmasked tumor-specific vulnerabilities, identifying cancer-cell-restricted regulators that fine-tune Wnt signaling outputs, offering promising avenues for selectively crippling oncogenic Wnt activity.59 For example, secreted frizzled-related proteins antagonize Wnt signaling by ligand sequestration, demonstrating tumor-suppressive effects in preclinical models through their peptide derivatives.60 v-ATPase upregulation drives Wnt/β-catenin-dependent tumorigenesis. The gene discussed is FRZB; the disease is neoplasm.