Bevacizumab combined with cytotoxic chemotherapy is that the backbone of metastatic colorectal cancer (mCRC) therapy; however, its treatment efficacy is hampered by therapeutic resistance. Therefore, understanding the mechanisms underlying bevacizumab resistance is crucial to increasing the therapeutic efficacy of bevacizumab. Cancer of the colon or rectum that has spread to other organs (metastatic colorectal cancer) is a commonly occurring disease that usually cannot be surgically removed. Bevacizumab is a humanized monoclonal antibody targeting vascular endothelial growth factor and thus inhibiting its interaction with vascular endothelial growth factor receptor. Furthermore, several studies have found that the addition of bevacizumab to chemotherapy could improve response rate and the rate of liver resection in patients with mCRC. Treatment composed of bevacizumab together with triplet (FOLFOXIRI) chemotherapy for induction (6-month maximum) therapy, followed by bevacizumab maintenance therapy, was assessed in 57 patients. The primary endpoint was PFS rate at 10 months from study entry; secondary endpoints included response rate and safety profile. The identified genes and pathways are often potential targets and predictors of therapeutic resistance and prognosis in bevacizumab-treated patients with mCRC.