In a murine model of hematopoietic progenitors with overexpressed oncogenic mutant Nras and deleted Cdkn2a (of note this is uncommon in ETP-ALL) abrogation of either Ezh2 or Eed led to a shorter ETP-ALL latency and deregulation of growth and survival signalling [17]. Here, EZH2 is linked to acute lymphoblastic leukemia.