RAS is a family of small GTPases and acts as an oncogene. Point mutations in codons 12 and 13 of RAS gene increases its affinity for GTP and those in codon 61 inactivate its autocatalytic GTPase function, resulting in permanent RAS activation and stimulation of its downstream targets along the MAPK and PI3K/AKT signaling pathways. In thyroid, RAS (HRAS, NRAS and KRAS) mutations are identified in 10--20% of papillary carcinomas, 40--50% of follicular carcinomas, 10% of medullary carcinomas, and 20--40% of poorly differentiated and anaplastic carcinomas. The frequency of HRAS mutations in thyroid carcinomas is approximately 4%. HRAS mutations at codon 61 have been reported in a variety of thyroid lesions and are especially prevalent in the follicular variant of papillary thyroid carcinoma. However, the predictive or prognostic significance of HRAS mutation in thyroid carcinoma is not clear and correlation with other clinical and laboratory findings is necessary.