Problems and Countermeasures of Molecular Targeted Therapy for Tumors In recent years, the research and clinical application of molecularly targeted drugs for tumors have elevated the level of tumor treatment to a new height. Nevertheless, there are still many problems to be solved in molecular targeted therapy of tumors. 1.1 Rituximab (rituxan) Rituximab can kill B-cells and reduce plasma cell production, which may cause patients to suffer from hypo-immunoglobulinemia, lung infections due to impaired immune function, and other toxic side effects. 1.2 Imatinib Research has found that imatinib can inhibit T-cell proliferation and activation in vitro; reduce the expression of T-cell and DC surface activity markers; inhibit DC differentiation and maturation; reduce cytokine secretion, and then inhibit T-cell immune response. 1.3 Dasatinib Research shows that dasatinib can inhibit T cell proliferation, activation and cytokine secretion, which has obvious inhibitory effect on the body’s immune function. 1.4 Sunitinib Sunitinib inhibits T-cell proliferation by blocking the cell cycle at the G0/G1 phase, inhibiting cytokine secretion, down-regulating the expression of cell-surface activity markers, and blocking Zap-70 protein signaling peptide. In order to ensure the efficacy of molecularly targeted therapy while reducing its impact on immune function, our center is currently conducting research on CIK/IL-2 combined molecularly targeted drug therapy. In addition, using adeno-associated viruses as vectors, the genes of human papillomavirus such as E6, E7 and GM-CSF have been transfected into DC for cervical cancer treatment, and the preliminary results show that it is safe and effective. At the same time, the BA/46 gene or mutant Her-2/Neu gene was transfected with DC for breast cancer treatment, and the experimental results showed that it could induce the production of CTL against specific antigens, and further clinical trials are in progress. 2, Efficacy prediction problems Studies have confirmed that non-small cell lung cancer patients with EGFR mutations are more sensitive to gefitinib treatment, and different mutation types have different responses to gefitinib treatment. In addition, studies have shown that K-ras mutations cause primary resistance to cetuximab in patients with colorectal cancer. However, in other tumors, similar studies are only in the preliminary stage, and there is still a lot of work to be done in order to achieve truly individualized treatment guided by molecular markers. 3, Drug resistance EGFR exon 20 T790M mutation combined with other mutations is one of the causes of gefitinib resistance, and T790M mutation is a marker of gefitinib resistance. In addition, tumor cells can activate the EGFR downstream signaling pathway through other receptor bypasses, causing EGFR inhibitor resistance to occur.PTEN dysfunction leads to persistent activation of the PI3K-AKT signaling pathway, which is potentially related to herceptin and cetuximab resistance. To address the issue of drug resistance, our center carried out a study to investigate the mechanism of cetuximab resistance in nasopharyngeal carcinoma at the cellular level. Preliminary results indicate that H-ras gene amplification and overexpression is one of the main mechanisms leading to cetuximab resistance in nasopharyngeal carcinoma, and the reason for its elevation is related to the over-activated IGF-1R signaling pathway. The related article has been published in Biomedicine & Pharmacotherapy. In conclusion, in order to realize the individualization of tumor treatment, the related issues of molecular targeted therapy deserve further in-depth research.