EZH2 and neoplasm: Interestingly, EZH2/RRAGC gain of function mutations and SESTRIN1 loss are mutually exclusive suggesting that these alterations are involved in mTORC1 activity maintenance allowing tumor cells to escape proliferation inhibition (84) also becoming less dependent to TFH signals as shown in the context of RRAGC and EZH2 mutations (83, 101).