Research has found that TERT accelerates the dedifferentiation and progression of BRAF mutant-induced THCA by regulating ribosome biogenesis[36] (studies indicate that focal adhesion kinase can drive the growth, invasion, and metastasis of THCA, promoting ribosome biogenesis, thereby driving the growth and survival of advanced THCA cells.[37] Prognostic studies in PTC have shown higher levels of OXPHOS in the tumor mutational burden group.[38] In most PTCs, OXPHOS complex I is significantly decreased (cells 2018, 7, 40[39]). Here, TERT is linked to neoplasm.