Given that BRAF/RAS mutations and RET/PTC rearrangements are mutually exclusive among themselves in the MAPK pathway and they each can independently activate the pathway, we speculated that RET/PTC, when coexisting with TERT promoter mutations, could, like BRAF/RAS mutations, also selectively upregulate the mutant TERT through activating the MAPK pathway, thus promoting tumor aggressiveness and poor clinical outcomes of PTC. This evidence concerns the gene TERT and neoplasm.