Unlike previously reported strategies that directly target oncogenic signaling within APC-truncated cells — such as inhibiting cholesterol biosynthesis (TASIN-1)21 or disrupting cholesterol-mediated Wnt activation through Dvl interaction22 — our study identified an immune-suppressive mechanism driven by APC and demonstrated that the APC11 peptide can restore anti-tumor immunity by blocking the PTPN13–STAT1 interaction. The gene discussed is DVL1; the disease is neoplasm.