Functionally, ITGA2 (integrin subunit α2) orchestrates a dysregulated signaling axis through β1‐integrin heterodimerization (α2β1), governing bidirectional extracellular matrix crosstalk that modulates neoplastic adhesion, metastatic motility, cancer stemness maintenance, and tumor angiogenesis.[32] While prior investigations established ITGA2 overexpression as an independent prognostic determinant in APTC,[33, 34] its pathogenetic role in pediatric thyroid carcinogenesis remained unresolved. The gene discussed is ITGA2; the disease is thyroiditis.