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Thyroid cancer is the most frequent endocrine cancer representing 1-1.5% of all cancers. Approximately 90% of these are differentiated thyroid carcinomas (DTC) with a favorable prognosis and cure rate. DTC has recently witnessed an increase in incidence with a relatively stable mortality rate, mostly due to intensive screening. Despite being considered indolent and the 10-year survival rate being above 90%, local or distant recurrence can be observed in up to 20% of cases. Mutations in BRAF, RET, RAS, NTRK1, PAX8-PPARG are commonly found in DTC but studies show that genetic alterations with apparently no correlation to DTC might improve or aggravate prognosis. Vitamin D deficiency and vitamin D receptor (VDR) gene polymorphisms is consider to be one of these factors, due to the fact that it exerts immunological and antineoplastic functions throught its antiproliferative and prodifferentiating actions. FokI gene polymorphism has been associated with later stage and negative prognosis in different studies. Also, polymorphisms of genes involved in folate metabolism (MTHFR, MTR, RFC1) may be incriminated in carcinogenesis, folate being an extremely important factor in DNA synthesis. Studies suggest that through correction and avoidance of incriminated neoplastic agents, thyroid cancer incidence, evolution and prognosis might improve significantly. For this to be possible we need to be aware of the molecular pathways these environmental factors use to exert their carcinogenic effects [ABSTRACT FROM AUTHOR]