Thyroid cancer is one of the common malignant tumors of the head and neck, accounting for 1%-2% of the malignant tumors in the whole body, mostly seen in women. Currently, thyroid cancer treatment is internationally divided into two groups: high-risk and low-risk, with different treatment responses. The main characteristics of the high-risk group include age older than 45 years, male, metastasis, tumor diameter greater than 4 cm, and extra-thyroidal invasion, and the treatment response is total thyroidectomy, radioisotope iodine (131I) therapy, thyroid stimulating hormone (TSH) suppression therapy, follow-up monitoring of thyroglobulin level and neck ultrasound, and radiotherapy for patients with recurrence or positive margins. The low-risk group was characterized by age less than 45 years, female, no metastasis, tumor diameter less than 4 cm, and no extra-thyroidal invasion, and was treated with total thyroidectomy, radioisotope 131I therapy, and follow-up thyroglobulin levels and ultrasound of the neck for patients with tumor diameter greater than 1 cm. The prognosis of thyroid cancer is closely related to the pathological stage, with a 5-year survival rate of more than 95% for stages I and II, about 90% for stage III, and about 50% for stage IV. In thyroid cancer, abnormal signaling molecules of cellular pathways are more common, and there are roughly two known abnormal transduction pathways, one is MAP kinase pathway, including abnormalities of BRAF (e.g. BRAF V600E, BRAF copy number amplification), PET/PTC, RAS and other genes; the other is PI3K/AKT pathway. Preclinical studies have shown that sorafenib, a multi-kinase inhibitor, inhibits multiple intracellular and cell surface kinases, including RAF kinase, VEGFR-2, PDGFR, RET and KIT, thus inhibiting the RAF/MEK/ERK signaling pathway on the one hand and blocking tumor neovascularization by affecting VEGFR and PDGFR on the other. On the other hand, it affects VEGFR and PDGFR to block the formation of tumor neovascularization and indirectly inhibit tumor cell growth. An open, phase II clinical trial conducted by Brose et al. evaluated the efficacy and safety of sorafenib in the treatment of metastatic thyroid cancer. Fifty-five patients who were insensitive to 131I therapy, had an expected survival >3 months, had disease progression within 6 months prior to enrollment, had a physical status (PS) score of 0 to 2, and had intact organ and bone marrow function were included in the study. These patients received oral sorafenib 400 mg twice a day and were evaluated by spiral CT every 2 months. The results showed that after 4 months of oral sorafenib, the patients had significantly better lung metastases or bone metastases. Of the 50 evaluable patients, 36% had partial remission (PR) and 46% had stable disease (SD), with a clinical benefit rate of 82% and a median PFS of 63 weeks and up to 84 weeks for those with good differentiation. The median OS at follow-up of 30 patients was 140 weeks, demonstrating the efficacy of sorafenib in patients with metastatic thyroid cancer who are not sensitive to 131I therapy. Previous studies have shown that thyroid cancer patients with BRAF V600E mutation (BRAF+) have significantly lower survival rates than BRAF wild-type (BRAF-) patients (p=0.015). However, in Rosen’s study, PFS was significantly longer in BRAF(+) patients than in BRAF(-) patients after taking sorafenib. In addition, patients had different levels of p-ERK, p-AKT, and p-S6 K expression at the time of progression after sorafenib. This study lays the foundation for a phase III clinical trial of sorafenib for metastatic thyroid cancer.