Thyroid carcinoma is the most common endocrine malignancy, with a rising global incidence. Simultaneously, the increased life expectancy of patients with transfusion-dependent thalassemia (TDT) has revealed new long-term complications, including an elevated risk of thyroid cancer. This epidemiological convergence raises the possibility of shared molecular mechanisms. In this review, we explore potential mechanistic associations between TDT and thyroid cancer, focusing on the oncogenic consequences of iron overload. Iron excess in TDT promotes a tumor-permissive environment via oxidative stress, chronic inflammation, and modulation of ferroptosis, a process with dual roles in tumor biology. These alterations contribute to DNA damage, genomic instability, and activation of oncogenic signaling cascades such as mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), while impairing immune surveillance. Iron-induced epigenetic remodeling and non-coding RNA dysregulation further support malignant transformation. Although a causal relationship remains unproven, the convergence of these pathways underscores the need for thyroid surveillance in thalassemia patients and supports targeted strategies addressing iron metabolism and ferroptotic vulnerability.