The classical function of TERT is to add telomeres at the end of chromosomes, preventing critical telomere shortening, thus enabling cancer cells acquire replicative immortality1. In addition to this function, recent studies have also established TERT as having powerful oncogenic functions in a telomere-independent manner. For example, overexpression of TERT mutant or a naturally occurring alternatively spliced variant of TERT lacking the reverse transcriptase activity stimulated cell proliferation in human and murine cells42,43. In fact, enforced TERT expression in transgenic mice promoted the development of spontaneous tumors44,45. Even expression of a TERT mutant that retained the catalytic activity but was incapable of maintaining telomere length promoted tumor formation in nude mice46. Moreover, TERT activated the RNA-dependent RNA polymerase activity47, increased cancer cell proliferation by promotes pol III-mediated expression of transfer RNAs48, and promoted cancer progression by regulating MYC stability and MYC-dependent oncogenesis49. The present study similarly demonstrated a robust oncogenic function of TERT and, importantly, its synergism with BRAF V600E in functioning this way.