Possible mechanisms for promotion of myeloid neoplasias by partial Myb deficiency. (A) WT HSCs balance self-renewal and differentiation to hematopoietic progenitor cells (HPCs). (B) Myb deficiency may enhance differentiation to myeloid HPCs, providing an increased target population for subsequent oncogenic events. (C) Proteostatic stress resulting from altered expression of MYB-regulated genes leads to compensatory proliferation or other prooncogenic changes favoring subsequent oncogenic events. Professional illustration by Somersault18:24.