RET and neoplasm: 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.