Core Viewpoint - The study highlights the role of Bacteroides fragilis in promoting chemoresistance in colorectal cancer (CRC) and suggests that targeting this bacterium with phage VA7 can restore chemosensitivity [1][4][10]. Group 1: Research Findings - Colorectal cancer (CRC) is the third most common cancer globally and the second leading cause of cancer-related deaths [1]. - Chemotherapy resistance is a major limitation in the treatment of metastatic CRC, and understanding the mechanisms behind this resistance is crucial for improving treatment strategies [1][3]. - Recent studies indicate that gut microbiota significantly influence tumor development and the efficacy of anticancer therapies [3]. Group 2: Mechanism of Chemoresistance - Bacteroides fragilis is found to be abundant in chemotherapy-resistant CRC patients, and its abundance correlates with poor prognosis [3][5]. - The bacterium weakens the efficacy of chemotherapy drugs such as 5-fluorouracil and oxaliplatin by binding to the Notch1 receptor in CRC cells, activating the Notch1 signaling pathway, and inducing epithelial-mesenchymal transition (EMT) [4][10]. - The study demonstrates that knocking out the SusD/RagB proteins of Bacteroides fragilis or blocking Notch1 signaling can eliminate the chemoresistance mediated by this bacterium [4][10]. Group 3: Therapeutic Implications - The research identifies phage VA7 as a specific agent that can target and eliminate Bacteroides fragilis, thereby restoring chemosensitivity in CRC mouse models [4][10]. - This study provides new insights into the potential of precision modulation of gut microbiota in the clinical treatment of colorectal cancer [7].