Core Viewpoint - Colorectal cancer (CRC) is the third most common cancer globally and the second leading cause of cancer-related deaths, with limited efficacy of immunotherapy in most cases [2] Group 1: Research Findings - A study published by Professor Zhou Weijie’s team reveals that APC deficiency inhibits CD8+ T cell infiltration and allows CRC to evade the immune response through PTPN13's dephosphorylation of STAT1, independent of the β-catenin pathway [3][6] - The use of an 11-amino-acid peptide from the C-terminus of APC (APC11) targets PTPN13, blocking the PTPN13-STAT1 interaction, promoting STAT1 phosphorylation, and enhancing the effectiveness of PD-1 blockade therapy [6][8] - The research uncovers a previously unknown APC/PTPN13/STAT1-dependent tumor immune suppression mechanism [7] Group 2: Implications for Treatment - The significant anti-tumor effects observed from the combination of anti-PD-1 antibodies and APC11 peptides provide important targets and theoretical foundations for the development of anti-tumor drugs for CRC patients [8]