SPI1 and myeloid neoplasm: Our results implicating a transforming role for sub-haploinsufficient levels of MYBL2 build upon earlier studies implicating progressive inactivation of CTNNA1 and the graded reduction of PU.1 expression in the molecular pathogenesis of myeloid malignancies (Rosenbauer et al., 2004; Liu et al., 2007).