Most of the genetic events implicated in the pathogenesis of thyroid cancer (TC) 
involve genes with kinase activity. Thus, kinase inhibitors (KIs) are very 
relevant in this field. KIs are considered the most suitable treatment for 
patients with iodine-refractory differentiated TC; these patients comprise the 
subgroup with the poorer prognosis. To date, only sorafenib has been approved 
for this indication, but promising results have been reported with several other 
KIs. In particular, lenvatinib has demonstrated excellent efficacy, with both 
progression-free survival and objective tumour response being better than with 
sorafenib. Despite being considered to be well tolerated, both sorafenib and 
lenvatinib have shown a remarkable toxicity, which has led to dose reductions in 
the majority of patients and to treatment discontinuation in a significant 
proportion of cases. The role of KIs in differentiated TC may be revolutionised 
by the finding that selumetinib may restore a clinical response to radioactive 
iodine (RAI). Vandetanib and cabozantinib have been approved for the treatment 
of advanced, progressive medullary TC (MTC). Nevertheless, the toxicity of both 
compounds suggests their selective use in those patients with strong disease 
progression. Treatment with the mTOR-inhibitor everolimus, alone or in 
combination with somatostatin analogues, should be studied in metastatic MTC 
patients with slow progression of disease, these representing the vast majority 
of patients. KIs did not significantly impact on the clinical features of 
anaplastic TC (ATC).