Existing models, relying on conventional clinical parameters (such as onset symptoms, tumor location, tumor burden, CEA level), pathological factors (histology, grading), and genetic molecular profiling (mutations in RAS, BRAF, HER2 gene amplifications, etc.), may not adequately capture the dynamic and heterogeneous nature of metastatic CRC, thus limiting their precision in predicting individual patient outcomes. Here, BRAF is linked to neoplasm.