Three proposed pathogenetic mechanisms could explain the coexistence of HT with DTC: (i) chronic inflammation, fostering malignant cell transformation through pro-inflammatory cytokines and growth factors; (ii) elevated TSH levels in HT patients progressing to hypothyroidism may stimulate thyroid epithelial cell proliferation; and (iii) a common genetic background, including RET/PTC gene rearrangement and p53 mutations, may also contribute to this association [8,9]. Here, RET is linked to hematocrit.