The tumor suppressor activity of BAP1 in myeloid progenitor cells was linked to its antagonism with PRC2, as the transformation of BAP1-deficient myeloid cells was associated with an increase in PRC2-mediated transcriptional repression and could be abolished by the loss or inhibition of the PRC2 catalytic subunit EZH2 (95, 96). This evidence concerns the gene EZH2 and neoplasm.