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in patients. Medullary thyroid cancer (MTC) derives from paraf- of 100, 93, 71, and 21 % for stages I, II, III, and IV Endocrine-Related Cancer (2012) 19 447–456(Pelizzo et al. 2007). Prognosis in patients with MTCollicular C-cells of the thyroid and comprisesw4 % of thyroid cancers in United States (Hundahl et al. 1998). MTC occurs in sporadic and hereditary forms. The heritable variants include three different clinical phenotypes: multiple endocrine neoplasia type 2A (MEN2A), MEN2B, and familial MTC-only syndrome respectively (Modigliani et al. 1998). Dominant activating mutations in the RET proto-oncogene have been identified as the underlying cause of the development of MTC (de Groot et al. 2006). The activation of antiapoptotic PI3K/AKT pathway and mitogenic MEK/ERK cascade are crucial events in cell transformation triggered by oncogenic RET (Segouf-Endocrine-Related Cancer (2012) 19 447–45