Thyroid cancer is a common endocrine malignancy with rising global incidence. Recent advances have elucidated key molecular mechanisms, including genetic and epigenetic alterations in signaling pathways such as MAPK and PI3K-AKT. These alterations, including mutations in BRAF, RAS, and RET, as well as gene copy-number gains and methylation changes, are critical for thyroid cancer development and progression. BRAF-V600E mutations are prevalent in papillary thyroid cancer (PTC) and associated with aggressive behavior, while RAS mutations are more common in follicular thyroid cancer (FTC). The PI3K-AKT pathway is also frequently altered, contributing to tumor growth and resistance to treatment. Other important mutations include CTNNB1, TP53, IDH1, ALK, and EGFR, which are linked to more aggressive thyroid cancers. Gene amplifications, such as those of PIK3CA and IQGAP1, also play a role in thyroid tumorigenesis. Translocations like RET-PTC and PAX8-PPARG are significant in thyroid cancer. Aberrant methylation of genes like PTEN and TIMP3 is common and contributes to tumor progression. The MAPK and PI3K-AKT pathways are central to thyroid cancer, with their activation driving tumor growth and metastasis. The NF-κB and WNT-β-catenin pathways also contribute to thyroid cancer progression. The TSH receptor signaling pathway is involved in thyroid cell proliferation and differentiation. Genetic and epigenetic alterations accumulate during thyroid cancer progression, with multiple mutations often co-occurring. The cooperation between MAPK and PI3K-AKT pathways is crucial for aggressive thyroid cancer. Impairment of the iodide-handling machinery in thyroid cells is a key factor in the resistance of thyroid cancer to radioiodine therapy. Recent advances in molecular understanding have led to new therapeutic targets, including MEK and BRAF inhibitors, and have improved diagnostic and prognostic tools for thyroid cancer. These findings highlight the complex molecular mechanisms underlying thyroid cancer and offer new opportunities for targeted therapies and improved patient outcomes.Thyroid cancer is a common endocrine malignancy with rising global incidence. Recent advances have elucidated key molecular mechanisms, including genetic and epigenetic alterations in signaling pathways such as MAPK and PI3K-AKT. These alterations, including mutations in BRAF, RAS, and RET, as well as gene copy-number gains and methylation changes, are critical for thyroid cancer development and progression. BRAF-V600E mutations are prevalent in papillary thyroid cancer (PTC) and associated with aggressive behavior, while RAS mutations are more common in follicular thyroid cancer (FTC). The PI3K-AKT pathway is also frequently altered, contributing to tumor growth and resistance to treatment. Other important mutations include CTNNB1, TP53, IDH1, ALK, and EGFR, which are linked to more aggressive thyroid cancers. Gene amplifications, such as those of PIK3CA and IQGAP1, also play a role in thyroid tumorigenesis. Translocations like RET-PTC and PAX8-PPARG are significant in thyroid cancer. Aberrant methylation of genes like PTEN and TIMP3 is common and contributes to tumor progression. The MAPK and PI3K-AKT pathways are central to thyroid cancer, with their activation driving tumor growth and metastasis. The NF-κB and WNT-β-catenin pathways also contribute to thyroid cancer progression. The TSH receptor signaling pathway is involved in thyroid cell proliferation and differentiation. Genetic and epigenetic alterations accumulate during thyroid cancer progression, with multiple mutations often co-occurring. The cooperation between MAPK and PI3K-AKT pathways is crucial for aggressive thyroid cancer. Impairment of the iodide-handling machinery in thyroid cells is a key factor in the resistance of thyroid cancer to radioiodine therapy. Recent advances in molecular understanding have led to new therapeutic targets, including MEK and BRAF inhibitors, and have improved diagnostic and prognostic tools for thyroid cancer. These findings highlight the complex molecular mechanisms underlying thyroid cancer and offer new opportunities for targeted therapies and improved patient outcomes.